Preterm Neonatal Resuscitation

Written by: Aaron Wibberley, MD (NUEM ‘22) Edited by: Vidya Eswaran, MD '20 Expert Commentary by: Spenser Lang, MD

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Expert Commentary

Thanks to Dr. Wibberley and Dr. Eswaran for providing this infographic on a tough topic – neonatal resuscitations.

Usually, deliveries in the emergency department cause a dichotomy of emotions – initial anxiety, then relief and happiness. Most of our deliveries tend to be quick, precipitous, with hopefully just enough warning for us to grab gloves and remember where the baby warmer is. Unfortunately, when babies decide to struggle with their first few minutes of life, this becomes a lot more stressful for everyone.

Fair warning – though I am an emergency medicine physician, and prepared to deal with emergent situations of any age, I think there are very few of us who feel as comfortable with neonatal resuscitations as we do with critically ill trauma or cardiac arrest patients. Especially if your department sees very little pediatrics, it is completely normal to feel anxiety when imagining resuscitating a neonate, and even more so a pre-term baby. This is OK! In fact, this should motivate you to get familiar with NRP, and provides a perfect opportunity for spaced repetition throughout your career to enhance recall.

Here are my broad strokes steps for a fresh neonate requiring resuscitation.

#1: Know your resources! The first step in managing a neonatal resuscitation occurs far before the patient shows up in your department. Where is your baby warmer? Where are your teeny-tiny BVM’s? What’s the smallest ETT and intubating blade you stock, and where?  I promise you, the hardest part of intubating this baby won’t be the actual mechanics of placing an ETT – it will be in the preparation and supply gathering. Don’t rely on your nurses to know everything when seconds count – know where this stuff is yourself.

#2: Call for help, early and often. Many emergency departments have some type of OB/imminent delivery response – hopefully this brings in a pediatrician well trained in neonatal resuscitation as well. Hopefully, this also brings a nurse who is used to placing IV’s in these itty bitty babies. If this doesn’t describe your hospital, call to start the transfer process, and move on to #3…

#3: Dry and stim. Nearly all babies respond to drying and stimulation. Please don’t start bagging a poor newborn before drying it off and giving it a good rub for 30-60 seconds (unless it’s extremely pre-term – try to avoid rubbing all the skin off of a 25-weeker, this is bad form.) At the same time, keep in mind that these babies will need some form of external thermoregulation so make sure the warmer is actually functioning.

#4: When in doubt, fix the breathing. As is obvious when scanning through NRP guidelines, 95% of managing a sick newborn lies in assisting the respirations. Poor tone? Fix the breathing. Initial HR below 100? Try to fix the breathing. Poor color? You get it. Don’t be afraid to escalate from blow by, to PEEP, to BVM. If the baby has little to no respiratory effort, a couple initial breaths via BVM can quickly improve the situation. But please, when you’re bagging a tiny neonate, use small breaths – this is not the typical 120 kg patient we are used to.

#5: In the short term, an IO is your friend. A UVC is golden, but not really possible in an active resuscitation. The good news is that most babies don’t need IV access in the short term – for my  reasoning, see #3 and #4. The literature suggests that placing the neonatal IO in the proximal tibia, distal tibia, or distal femur can be safe and effective.

#6: This is the time to debrief. Whether a happy or a tragic ending, this is a rare and emotional event in the emergency department. Debrief with your team. Talk to whoever you talk to about this stuff – spouse, friend, coworker. We are champions of compartmentalization in the emergency department out of necessity, but don’t bear the entirety of these encounters on yourself – lean on those around you.

Spenser Lang, MD

Assistant Professor

Department of Emergency Medicine

University of Cincinnati

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Wibberly, A. Eswaran, V. (2020, Nov 9). Preterm Neonatal Resuscitation. [NUEM Blog. Expert Commentary by Lang, S]. Retrieved from http://www.nuemblog.com/preterm-neonatal-resuscitation

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A “Pill-in-the-Pocket” Approach to Paroxysmal Atrial Fibrillation

Written by: David Feiger, MD (NUEM ‘22) Edited by: Jon Andereck, MD, MBA NUEM ‘19) Expert Commentary by: Kaustubha Patil, MD

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The Case

A healthy 65-year-old male with paroxysmal atrial fibrillation presents to the emergency department in atrial fibrillation with rapid ventricular rate. His blood pressure is 135/83, heart rate 135, respirations 15 with an O2 saturation of 98% on room air. He states that he took his “pill-in-the-pocket” four hours prior to presentation and his symptoms did not resolve.

Atrial fibrillation

A study in the Western Journal of Emergency Medicine in 2013 observed the costs associated with emergency department (ED) treatment and discharge of patients presenting with atrial fibrillation (AF) or atrial flutter was $5,460 [10]. Those admitted to the hospital naturally incur far higher costs. For those eligible, a visit to the ED could be avoided with the “pill-in-the-pocket” approach.

What is the “pill-in-the-pocket” approach?

The “pill-in-the-pocket” approach is the administration of a prescribed class IC antiarrhythmic, either flecainide or propafenone, following recent onset of episodes of palpitations in patients with paroxysmal AF. It is generally initiated by the patient’s cardiologist after extensive cardiac evaluation to rule out structural disease and other conduction abnormalities. The idea is to terminate the suspected episode of AF without having to present to an ED or clinic. Several studies have investigated the safety of this approach and supported this method of outside-the-hospital termination of paroxysmal AF events [2, 14].

Who is eligible for the “pill-in-the-pocket” approach?

In a study in the New England Journal of Medicine supporting the feasibility and safety of this out-of-hospital treatment, only specific patients were selected to participate. Inclusion criteria included:

• healthier patients between 18 and 75 years old

• a history of infrequent AF not associated with chest pain, hemodynamic instability, dyspnea, or syncope

• no significant electrocardiographic abnormalities (pre-excitations, bundle branch blocks, long QT interval, etc.)

• no structural or functional cardiac diseases

• no history of thromboembolic episodes

• no current use of an antiarrhythmic medication

• not currently pregnant

• no significant chronic disease including but not limited to muscular dystrophies, systemic collagen disease, and renal or hepatic insufficiency

These patients were then admitted to the hospital for a cardiac workup and were trialed on either flecainide or propafenone with successful pharmacologic cardioversion in the inpatient setting. Both flecainide and propafenone are proarrhythmic, thus structural heart diseases must be ruled out before their use and patients should be monitored during initiation of therapy [2].

How do flecainide and propafenone work?

Flecainide and propafenone are both powerful class IC antiarrhythmics that strongly bind fast sodium channels with a slower association and dissociation than other class I antiarrhythmics. These drugs slow phase 0 during sodium-dependent depolarization in cardiac muscle cells of the atrial and ventricular myocardium (Figure 1). This effect is primarily important in prolonging atrial refractoriness, thus aiding in the conversion and termination of AF. Flecainide’s use in tachyarrhythmias comes from its rate-dependence property in which its efficacy is greater at faster heart rates. Propafenone has additional beta blocker activity which may enhance its overall clinical effectiveness in treating tachyarrhythmias [3, 5, 6, 13].

What are treatment options for patients presenting to the ED in AF?

For all comers presenting in AF with rapid ventricular rate to the ED, the literature has not elicited a perfect treatment modality, and no distinction is made for patients on the “pill-in-the-pocket” approach prior to arrival. Despite this, general practice guidelines are highlighted in many textbooks.

In hemodynamically-stable patients, rate control in the ED is the generally the treatment of choice. Diltiazem is often preferred as compared to beta blockers like metoprolol, which may cause hemodynamic instability in patients with underlying heart or lung disease. In otherwise healthy patients, metoprolol is a reasonable choice [1]. Digoxin is also appropriate, but onset takes several hours and is inferior to beta-blockers for rate control within 6 hours of treatment [11].

Patients who have been in AF for > 48 hours are at a greater risk of new intracardiac thrombus formation and cardioversion-induced embolization. Newer data from a study in 2014 suggests that there is an increased risk of thrombus formation with > 12 hours of AF [8] though the original guidelines for electric cardioversion within 48 hours of symptom onset have not changed. Patients who are hemodynamically stable who have been in AF for > 48 hours (and considered if > 12 hours) should be admitted from the ED for transesophageal echo to rule out intracardiac thrombus prior to cardioversion, or alternatively for initiation of anticoagulation [7].

In hemodynamically unstable patients, electrical cardioversion should be pursued regardless of a patient’s anticoagulation status [7].

Are there any treatment considerations in the ED for patients in AF taking flecainide or propafenone?

Treatment failure to the “pill-in-the-pocket” approach may be a marker of progression of the patient’s clinical disease. However, if a patient presents within an hour or two of taking their “pill-in-the-pocket,” remember the four to six-hour onset of these medications suggests they may convert during their ED stay. As in the case initially presented, the patient spontaneously converted while waiting for a provider. For those that do not, these patients warrant evaluation for new structural cardiac disease and may no longer benefit from the “pill-in-the-pocket” approach and may require daily maintenance prophylactic therapy [2].

A subset of stable patients presenting to the ED with AF with rapid ventricular rate may be taking flecainide or propafenone as maintenance therapy and not as part of the “pill-in-the-pocket” approach. In this instance, some literature has suggested that these patients can take an extra dose or two up to the maximum daily dose of flecainide (400mg) or propafenone (900mg for immediate release and 850mg for sustained release) to attempt pharmacological conversion, and it would be reasonable to attempt this in the ED [9].

To admit or not admit, that is the question.

The patient’s clinical picture should guide the provider as to the patient’s disposition. A patient’s comorbidities, current stability following conversion to normal sinus rhythm, plan for possible ablation, necessity for starting anticoagulation or maintenance medication, and means for close cardiology or PCP follow up on an outpatient basis should be factored when dispositioning the patient. Certainly, if a patient is requiring continuous IV infusion of rate controlling medications or has poor rate control, he or she should be admitted to the hospital [1]. Recent literature suggests that discharging stable patients home is safe following successful electrical, pharmacologic, or spontaneous cardioversion in the ED [4].

Final Thoughts

The “pill-in-the-pocket” approach is a great way for eligible patients to self-terminate episodes of AF in the comfort of their home, potentially preventing a costly and lengthy ED visit. While this approach has been shown to be a safe and effective for terminating paroxysmal AF, there is a significant lack of data on how to treat these patients who do not respond to these medications at home. General principals should be followed–electric cardioversion if the patient is hemodynamically unstable and rate control medications if the patient is hemodynamically stable (or rhythm control if you happen to practice in Canada [14]. Patients may be discharged home with close cardiology or PCP follow up if successfully cardioverted.

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Expert Commentary

Atrial fibrillation (AF) is the most common cardiac arrhythmia and worldwide prevalence and incidence are increasing.1 It is estimated that by 2050 more than 12 million Americans will suffer from this debilitating and dangerous arrhythmia.1-2  AF presentations to Emergency Departments are certainly not without cost and the overall burden on the healthcare system will undoubtedly increase as the prevalence of atrial fibrillation continues to rise. A “pill in the pocket” approach for treatment of symptomatic atrial fibrillation has been well-described.

Class IC (sodium channel blockers) antiarrhythmic drugs (flecainide and propafenone) are the drugs of choice for “pill in the pocket” chemical cardioversion of symptomatic atrial fibrillation. There are some important considerations for this approach to be safe and effective:

1. The patient should have a history of infrequent paroxysmal atrial fibrillation, not persistent atrial fibrillation (episodes of AF that last greater than 7 days).

2. We reserve this approach for patients with symptomatic atrial fibrillation (palpitations, mild dyspnea, or mild lightheadedness) with rapid ventricular rates who do not experience dangerous symptoms such as chest pain or syncope.

3. As anti-arrhythmic drugs can also be pro-arrhythmic, we do not recommend Class IC antiarrhythmic drugs in patients with known structural heart disease, reduced left ventricular systolic function, or known coronary artery disease, due to the increased risk of inducing dangerous arrhythmias.

4. In patients who are not on therapeutic anticoagulation, we only recommend this approach when it has been less than 24 hours since onset of the AF episode. If the AF episode has lasted beyond 24 hours or it is unknown when the episode started, the risk of formation of intracardiac thrombus during AF and subsequent risk of stroke after a successful chemical cardioversion from a Class IC drug would be prohibitively high.

5. Due to the use-dependent nature of Class IC antiarrhythmics (more effective with more sodium channel blockade at faster ventricular rates), there is a chance of slowing conduction throughout the heart to the point that atrial fibrillation can organize into rapid atrial flutter with 1:1 AV conduction, leading to an aberrant wide complex tachycardia. For this reason, we recommend that the patient receive a beta-blocker or calcium channel blocker at least 30 minutes prior to administration of flecainide or propafenone.

6. Some practitioners recommend that if the patient is not already on anticoagulation, that they initiate anticoagulation at the time of beta-blocker or calcium channel blocker administration to reduce the risk of intracardiac thrombus formation if the patient does not convert to sinus rhythm within 24-48 hours.

7. Some practitioners recommend that the first attempt at “pill in the pocket” dosing be performed in the emergency department so that safety and efficacy can be monitored.

8. If patients report a progressively increasing need for “pill in the pocket” use or there is a suggestion of increasing burden of AF episodes, I recommend consultation with the patient’s cardiologist or electrophysiologist to discuss alternative options for rhythm control of symptomatic atrial fibrillation. Potential options at that time could include initiation of maintenance antiarrhythmic drug therapy versus invasive management with catheter ablation of atrial fibrillation. 

When used in the right patient, a “pill in the pocket” approach can be a very effective strategy for rhythm control of infrequent symptomatic paroxysmal atrial fibrillation. Appropriate patient factors to consider prior to recommending this approach are nicely highlighted in the post above. “Pill in the pocket” management for AF can resolve patient symptoms, improve patient’s quality of life, and reduce unnecessary emergency room visits and subsequent hospitalizations.

References

1. Chugh SS, Havmoeller R, Narayanan K, et al. Worldwide epidemiology of atrial fibrillation: a Global Burden of Disease 2010 Study. Circulation. 2014 Feb 25; 129(8):837-47.

2. Miyasaka Y, Barnes M, Gersh B, et al. Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence. Circulation. 2006 Jul 11;114(2):119-25.

Kaustubha Patil, MD

Clinical Cardiac Electrophysiology

Bluhm Cardiovascular Institute Northwestern Medicine

Assistant Professor of Medicine

Northwestern University Feinberg School of Medicine

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Feiger, D. Andereck, J. (2020, Nov 2). A “Pill-in-the-Pocket” approach to paroxysmal atrial fibrillation. [NUEM Blog. Expert Commentary by Patil, K]. Retrieved from http://www.nuemblog.com/blog/pill-in-pocket.

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References

1. Adams, James, et al. “Tachydysrhythmias.” Emergency Medicine: Clinical Essentials, Elsevier Health Sciences, 2013, pp. 497–513.

2. Alboni, Paolo, et al. “Outpatient Treatment of Recent-Onset Atrial Fibrillation with the ‘Pill-in-the-Pocket’ Approach.” New England Journal of Medicine, vol. 351, no. 23, 2004, pp. 2384–2391., doi:10.1056/nejmoa041233.

3. Aliot, E., et al. “Twenty-Five Years in the Making: Flecainide Is Safe and Effective for the Management of Atrial Fibrillation.” Europace, vol. 13, no. 2, 2010, pp. 161–173., doi:10.1093/europace/euq382.

4. Besser, Kiera Von, and Angela M. Mills. “Is Discharge to Home After Emergency Department Cardioversion Safe for the Treatment of Recent-Onset Atrial Fibrillation?” Annals of Emergency Medicine, vol. 58, no. 6, 2011, pp. 517–520., doi:10.1016/j.annemergmed.2011.06.014.

5. Dan, Gheorghe-Andrei, et al. “Antiarrhythmic Drugs–Clinical Use and Clinical Decision Making: a Consensus Document from the European Heart Rhythm Association (EHRA) and European Society of Cardiology (ESC) Working Group on Cardiovascular Pharmacology, Endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and International Society of Cardiovascular Pharmacotherapy (ISCP).” EP Europace, vol. 20, no. 5, 2018, doi:10.1093/europace/eux373.

6. Dukes, I.d., and E.m Vaughan Williams. “The Multiple Modes of Action of Propafenone.” European Heart Journal, vol. 5, no. 2, 1984, pp. 115–125., doi:10.1093/oxfordjournals.eurheartj.a061621.

7. January, Craig T., et al. “2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation.” Journal of the American College of Cardiology, vol. 64, no. 21, 2014, doi:10.1016/j.jacc.2014.03.022.

8. Nuotio, Ilpo, et al. “Time to Cardioversion for Acute Atrial Fibrillation and Thromboembolic Complications.” Jama, vol. 312, no. 6, 2014, p. 647., doi:10.1001/jama.2014.3824.

9. “Pill-in-a-Pocket Dosing Safely Converts Breakthrough Atrial Fib.” Family Practice News, vol. 35, no. 18, 2005, p. 20., doi:10.1016/s0300-7073(05)71733-3.

10. Sacchetti, Alfred, et al. “Impact of Emergency Department Management of Atrial Fibrillation on Hospital Charges.” Western Journal of Emergency Medicine, vol. 14, no. 1, 2013, pp. 55–57., doi:10.5811/westjem.2012.1.6893.

11. Sethi, Naqash J., et al. “Digoxin for Atrial Fibrillation and Atrial Flutter: A Systematic Review with Meta-Analysis and Trial Sequential Analysis of Randomised Clinical Trials.” Plos One, vol. 13, no. 3, 2018, doi:10.1371/journal.pone.0193924.

12. Stiell, Ian G., et al. “Association of the Ottawa Aggressive Protocol with Rapid Discharge of Emergency Department Patients with Recent-Onset Atrial Fibrillation or Flutter.” Cjem, vol. 12, no. 03, 2010, pp. 181–191., doi:10.1017/s1481803500012227.

13. Wang, Z, et al. “Mechanism of Flecainide's Rate-Dependent Actions on Action Potential Duration in Canine Atrial Tissue.” American Society for Pharmacology and Experimental Therapeutics, vol. 267, no. 2, 1 Nov. 1993, pp. 575–581.

14. Yao, R., et al. “Real-World Safety And Efficacy Of A ‘Pill-In-The-Pocket' Approach For The Management Of Paroxysmal Atrial Fibrillation.” Canadian Journal of Cardiology, vol. 33, no. 10, 2017, doi:10.1016/j.cjca.2017.07.371.

Management of Snake Bite Injuries

Written by: Rafael Lima, MD (NUEM ‘23) Edited by: Mike Conrardy, MD (NUEM ‘21) Expert Commentary by: Sean Bryant, MD

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An estimated 10,000 patients visit emergency departments for snake bite injuries each year in the United States [1]. The number of snake bite occurrences an emergency department sees depends largely on the geographic area of practice. While there are known remedies for these incidents, snake bites can be devastating if not promptly managed, meaning emergency physicians should be knowledgeable in the subject. In this article, we review the common management of snake bite injuries and envenomations for the two major snake groups in the United States.

Overview

There are about 20 known venomous species of snakes in the United States. While most envenomations occur in the Southwestern United States, every region is home to at least one species of venomous snake [2]. Not all snake bites result in envenomation. At least 25% of venomous snake bites are dry. You should still suspect envenomation upon the patient’s initial presentation and rule it out by monitoring their clinical symptoms and progression.

Identification of the snake is useful in guiding management of care, but it should not be attempted if doing so poses any additional risk to the patient or provider. In the United States, venomous snakes generally fall under two categories: Crotaline/pit vipers in the Viperidae family, and coral snakes in the Elapidae family.

Crotaline (Pit Vipers)

This group of snakes has historically been responsible for the more severe envenomations between the two groups [3]. The WHO classifies pit vipers in CAT 1 of their venom database, describing them as highly venomous with high rates of morbidity and mortality [4].

Pit vipers generally have a triangular shaped head with heat-sensing “pits” located on the face. They frequently have a rattle on their tail, but not all pit vipers are rattlesnakes. Copperheads and cottonmouth snakes are also included in this group.

Crotaline venom causes localized tissue necrosis and congestive coagulopathy. This can be identified by a prolonged INR, PT, PTT, and thrombocytopenia. Additionally, the viper venom can cause capillary and cellular membranes to increase in permeability. Large amounts of venom can cause diffuse vaso-extravasation and hemolysis that can lead to hypovolemic shock and DIC if untreated.

CroFab is the antivenom of choice for cotaline envenomation. It is a polyvalent antivenom, meaning it contains antibodies derived from the venom of multiple different species of snakes. Administration is titrated based on clinical and symptom response.

Elapidae

The venomous Elapidae snake in the United States is the coral snake. There are less severe envenomations from coral snakes compared to pit vipers. This is a result of how venom is administered between the two groups: pit vipers have venom glands that inject venom directly through the fangs, while coral snakes rely on passive seeping of venom through their glands while they chew.

Source: Tad Arensmeier from St. Louis, MO, USA

Coral snakes can be identified by their brightly colored rings extending along the length of the whole body. Usually, every other ring is yellow, separating the wider red or black rings in between. The common saying “red on yellow, kill a fellow; red on black, venom lack” has been been used to differentiate between venomous coral snakes and their harmless look-alikes in North America. A further level of differentiation is how far the rings extend circumferentially around the snake. Rings encircle the entire body in venomous coral snakes, while harmless look-alikes do not have the red coloration on the ventral side [5].

Source: Dawson at English Wikipedia

Venomous bites by coral snakes usually elicit little to no pain. This is because the Elapidae venom acts upon the neuromuscular junction and inhibits acetylcholine receptors. Clinical manifestations are predominantly neurological. Envenomation can cause lethargy, confusion, salivation, cranial nerve palsies, and respiratory paralysis. Symptoms are usually delayed, up to 12 hours from the initial bite. Coagulopathy and tissue necrosis does not happen with coral snake venom [2]. Unfortunately, the Elapidae antivenom is no longer manufactured in the United States and there is a limited supply available.

 ED Work Up

As in all patients who present to the emergency department, first ensure that airway, breathing, and circulation are intact. All suspected snake bite injuries warrant a prompt toxicology or poison center consult.

Sometimes, patients will bring in a dead or decapitated snake for identification in the emergency department. DO NOT attempt to handle a snake the patient brought in for identification, even if it is dead. Many snakes have intact reflexes that are preserved even after death or decapitation and you can still be bitten and envenomated by a dead snake!

Examine the injury and look for clear fang marks or puncture wounds. Get a history focused on the timing of the injury, medication allergies, and description of the snake, if known. The borders of erythema should be measured and marked serially.

Laboratory work-up is focused on assessing coagulopathy and hemolysis, especially if the snake is a confirmed pit viper or is unknown. Obtain CBC with platelet count, PT, PTT, INR, fibrinogen, and D-dimer. It is also important to check a baseline set of electrolytes with a basic chem panel, assess the extent of myonecrosis with a CK, and assess for renal damage with a UA.

Manage the wound with copious irrigation and exploration for retained foreign bodies (ie. fangs or teeth). Inquire about the patient’s tetanus status and administer if they are not up to date. Do not attempt to tourniquet or suction venom out of the wound. There is no evidence for routine antibiotic use in snake injuries [6].

Crotaline Bite Management

Consider using CroFab antivenom if the local area of injury and erythema is expanding. If coagulopathy is detected, do not treat with heparin or FFP. Give antivenom first, as unneutralized venom will react with clotting factor replacements [2]. Patients with abnormal coagulation studies within 12 hours after CroFab administration are more likely to develop recurrent coagulopathy. In these patients, repeat coagulation studies should be obtained every 48 hours until resolved. If lab values are worsening, then antivenom retreatment should be reconsidered [7].

Observe the affected limb for compartment syndrome. If clinical suspicion is high for compartment syndrome, consider formally measuring compartment pressures. Elevate the affected limb, and administer extra vials of antivenom. Antivenom administration is preferred over fasciotomy in the treatment of compartment syndrome caused by Crotaline venom [8].

Crofab, the Crotaline antivenom, is typically administered in stepwise fashion and is titrated to clinical resolution of symptoms. Administer 4-6 vials of CroFab antivenom and watch for clinical improvement at the local site of injury. If no improvement seen, administer 4-6 more vials. Repeat until control is achieved, meaning a reversal of symptoms, such as erythema, swelling, pain. Then administer 2 vial doses 6 hours later, then 12 hours, then 18 hours. Envenomation patients should be monitored for at least 8 hours. Keep epinephrine and antihistamines nearby in case of anaphylaxis or allergy to antivenom [2].

Elapidae Bite Management

Because of their potential devastating neurologic effects, coral snake bites should be empirically treated with antivenom and monitored for respiratory deterioration. Provide good supportive care, including intubation and ventilation, if necessary. Avoid opioids for pain management as they may mask symptoms of impending neurologic manifestations. Patients with suspected coral snake envenomations should be monitored for 12 hours after the initial bite [2].

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Expert Commentary

Thank you, Dr. Lima for bringing the important and timely topic of snakebites to the table by posting this excellent overview!  Current poison center data (2018 National Poison Data System) indicate a total of 4,013 crotalid exposures with the majority being copperheads.  While morbidity is worrisome, mortality was fortunately low in our country with only one fatality reportedly from a rattlesnake [1].

Prehospital snakebite management has been an area of deserved scrutiny.  Limb immobilization, analgesia, and transport to a medical facility are critical actions.  Tourniquets, pressure immobilization bandages, cryotherapy, electrotherapy, and incision/suction are not recommended and are likely harmful.  One researcher discovered that venom extraction suction devices “just suck” [2].  Having a cell phone in the field is most important to prevent loss of limb or life!

In other regions of the world, capturing or killing the snake may be optimal in determining which species specific antivenom to administer.  For North American crotalids, however, this practice is discouraged and exceedingly dangerous.  Both CroFab and Anavip (recently approved and now marketed with the goal of reducing risks of late coagulopathy) are prepared from several species of North American crotalids and can be used to manage any crotalid envenomation.  These contemporary antivenoms (Fab fragments) are safer than older polyvalent antivenom that resulted in high rates of anaphylaxis. 

Consult your regional poison center (1-800-222-1222) or staff medical toxicologist when managing snakebites!  For the number of snakebites that present to the emergency department, poison centers manage severalfold more each year.  Making decisions regarding the management of a limb that resembles compartment syndrome (more antivenom vs. surgical consultation), the interpretation of laboratory results, redosing of antivenom to gain initial control of swelling, and the management of nonindigenous (e.g. cobras, gaboon vibers) pet snakebites are nuances your subspecialists would love to collaborate on!

References

1. Gummin DD, Mowry JB, Spyker DA, BrooksDE, Beuhler MC, RiversLJ, Hashem HA, & Ryan ML 2018 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 36th Annual Report, Clinical Toxicology, 2019;57:1220-1413.

2.  Bush SP.  Snakebite Suction Devices Don’t Remove Venom: They Just Suck.  Annals of Emergency Medicine, 2004;43:187-188.

Sean Bryant, MD

Assistant Director, Toxicology Fellowship Program, Department of Emergency Medicine, Cook County Health

Associate Professor, Department of Emergency Medicine, Rush Medical College

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Lima, R. Cornardy, M. (2020, Oct 26). Management of Snake Bite Injuries. [NUEM Blog. Expert Commentary by Bryant, S]. Retrieved from http://www.nuemblog.com/blog/snake-bites.

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References

1. Snakebite Injuries Treated in United States Emergency Departments, 2001–2004. O’Neil, Mary Elizabeth et al. Wilderness & Environmental Medicine, Volume 18, Issue 4, 281 - 287

2. Gold, Barry S., et al. “Bites of Venomous Snakes.” New England Journal of Medicine, vol. 347, no. 5, 1 Aug. 2002, pp. 347–356., doi:10.1056/nejmra013477.

3. Seifert, Steven A., et al. “AAPCC Database Characterization of Native U.S. Venomous Snake Exposures, 2001–2005.” Clinical Toxicology, vol. 47, no. 4, 2009, pp. 327–335., doi:10.1080/15563650902870277.

4. “Venomous snakes distribution and species risk categories.” World Health Organization. 2010. http://apps.who.int/bloodproducts/snakeantivenoms/database/

5. Cardwell, Michael D. “Recognizing Dangerous Snakes in the United States and Canada: A Novel 3-Step Identification Method.” Wilderness & Environmental Medicine, vol. 22, no. 4, 1 Oct. 2011, pp. 304–308., doi:10.1016/j.wem.2011.07.001.

6. Prophylactic Antibiotics Are Not Needed Following Rattlesnake Bites. August, Jessica A. et al. The American Journal of Medicine, Volume 131, Issue 11, 1367 - 1371

7. Recurrence phenomena after immunoglobulin therapy for snake envenomations: Part 2. Guidelines for clinical management with crotaline Fab antivenom. Annals of Emergency Medicine, 2001, Vol.37(2), p.196-201., doi: 10.1067/mem.2001.113134

8. Hall, Edward L. “Role of Surgical Intervention in the Management of Crotaline Snake Envenomation.” Annals of Emergency Medicine, vol. 37, no. 2, Feb. 2001, pp. 175–180., doi:10.1067/mem.2001.113373.

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U Tox: Clinical Utility and False Negatives

Written by: Ben Kiesel , MD (NUEM ‘23) Edited by: Jason Chodakowski, MD (NUEM ‘19) Expert Commentary by: Joe Kennedy, MD

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Expert Commentary

The urine drug screen is one of the most frequently ordered and more frequently cursed tests in all of medicine.  It is one of the few tests that generates more argument than the banal discussions between surgeons and emergency physicians regarding the utility of a white blood cell count.  Nevertheless, in skilled hands, this cheap and simple immunoassay can answer a few quick questions.  The key is in knowing your Achilles heel:

1. Opioids and opiates produce similar toxidromes, but there are virtually limitless combinations of street and prescription drugs, lab assays, and confirmatory tests to tell these apart.  If the test is negative, who cares! Treat the patient in front of you.  Fentanyl and its analogues are perhaps most often missed.  Wake the patient up, discuss their substance use, and move on. 

2. Hopefully you noticed that *many* things other than phencyclidine can lead to a positive urine drug screen for PCP.  Ever have a conversation with the mother of a 12 year old about their PCP use?  Best go into that conversation knowing that many other substances cross-react.  Perhaps the kid is actually on lamotrigine for seizures, and that is why they were combative.  Or perhaps like most humans, they took a few ibuprofen at some point.  Either way—when child protective services is consulted for a positive result, either call the poison center or your local toxicologist for help.

Perhaps the most important point is that this is a screen and absolutely by no means a confirmatory test.  When it matters (placement, custody, fired/hired, transplant eligibility, excluding other diagnoses), get an actual level or result.  Not sure how to do that?  Call your lab!  Or call me.  Toxicologists love solving these problems and teaching and helping others do the same!

Joe Kennedy, MD

Attending Physician, Emergency Medicine

University of Illinois Hospital

Senior Toxicology Fellow

Toxikon Consortium

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Kiesel, B. Chodakowski, J. (2020, Oct 19). U Tox: Clinical Utility and False Negatives. [NUEM Blog. Expert Commentary by Kennedy, J]. Retrieved from http://www.nuemblog.com/blog/utox-clinical-utility-and-false-negatives.

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Peripheral Vasopressors: Do I need that central line?

Written by: Saabir Kaskar, MD (NUEM ‘23) Edited by: Abiye Ibiebele, MD (NUEM ‘21) Expert Commentary by: Marc Sala, MD

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Vasopressors have been used to treat shock since the early 1900s and continue to remain a mainstay of management of distributive shock. Traditionally, these medicines have been delivered through central venous catheters primarily due to the perceived risks of peripheral infusion, which include potential extravasation of vasoactive medicines and subsequent tissue necrosis. However, central venous catheter insertion is accompanied by its own risks such as pneumothorax, infection and carotid artery insertion and dilation. There is also a risk to delaying vasopressor initiation in hypotensive patients which is why vasopressors are often now started peripherally until central access can be attained.

Peripheral administration of vasopressors has classically been reserved for less potent vasoconstrictors such as phenylephrine and vasopressin. Fear of extravasation and tissue injury often is a cause for concern prior to starting norepinephrine, epinephrine or dopamine peripherally. The perceived harm from administrating these medicines peripherally largely stems from case reports over the past 60 years. However, what does the latest evidence tell us? Is this fear warranted or is it just a myth? Can we send our patients in shock up to the ICUs without central access?

One prospective observational study conducted at Long Island Jewish Medical Center evaluated the safety of vasoactive medication administered through peripheral IV sites. [1] The study monitored the use of vasopressors (norepinephrine, dopamine, and phenylephrine) in an intensive care unit with a total of 734 patients observed. The study incorporated an interdisciplinary protocol between pharmacy, nursing, physicians for administering vasoactive medicines through a peripheral IV. The protocol required that nursing staff examine the PIV access site every two hours, IV size be either 18 or 20 gauge, and utilize upper extremity vein sites with over 4mm vein diameter visualized via ultrasound. During the time of the study, 783 out of 953 patients received vasopressors for 49 +/- 22 hours through peripheral IV. While anatomic position of access site was not formally recorded, most IVs were placed in the upper arm basilic or cephalic vein. Peripheral vasopressors were only allowed to run for 72 hours before running centrally. Of the 783 patients, infiltration of the PIV occurred in 19 (2%) patients. All 19 had prompt local injection of phentolamine and application of nitroglycerin paste at the site of extravasation. No tissue injury was noted at the site of extravasation in any of the 19 cases.

This study shows that administration of vasopressors peripherally is feasible with a low risk if proper precautions are taken. The risk of extravasation and tissue necrosis is still present especially in ED’s and ICUs where such rigorous protocols are not in effect. However, this study demonstrates that vasopressor use may not be an automatic indication for central venous catheter insertion.

A more recent systematic review of peripheral vasopressor safety was recently published in Emergency Medicine Australia. [2] The review incorporated seven observational studies, roughly 1300 patients, that reported the incidence of adverse events for the continuous infusion of peripheral vasopressors including the above study.  The major finding was that extravasation events were uncommon (3.4%) and that no significant tissue necrosis or distal ischemia was reported. However, the data analyzed in this review comes from studies with mixed methodology quality and with limited duration of infusion. Five of the seven studies had peripheral vasopressor administration for less than 24 hours.

At its current state, the quality of data reviewing the safety profile of peripheral vasopressors is not universally high. However, the observational data we do have reports low incidence of complications which should be reassuring for clinicians especially when starting these medicines for short periods of time and as a bridge to possible central infusion. Early peripheral infusion should be given more consideration as delaying vasopressor administration has been shown to increase mortality in septic shock. [3] While further research is certainly needed in this field, the current state of data should at least quell some concerns of the perceived risks of peripheral vasopressor administration.

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Expert Commentary

Dr. Kaskar does a great job summarizing several of the major studies that can inform how we approach the infusion of peripheral vasoactive drugs in lieu of a central catheter. I can only assume we could agree one area of common ground, which is that if central access is in place, this should be used for the vasoactive infusion, given that the occurrence of tissue complications, while probably rare, can be limb-threatening.  An additional prospective study I would mention is by Medlej et al [1] where the authors prospectively studied ED patients managed for a variety of shock states with peripherally administered vasoactive agents and found that 3/55 (5.45% of total, and 6% of those receiving norepinephrine) had extravasation.  None had serious complications, but notably among the three events, all three used 20G IVs and two occurred using hand veins. This relatively small and heterogeneous study would indicate that extravasation is uncommon and when it occurs, is not particularly morbid, even with norepinephrine. 

Finally, another recent study notable for its cohort took place in the operating room context. Here, medical records of over 14,000 patients who received peripheral norepinephrine to manage hypotension associated with general anesthesia in two European academic centers were studied retrospectively for complications. Only five patients (0.035%) had extravasation, wherein the median infusion duration was 20 minutes, and none of whom had a significant complication from the extravasation. They calculated an estimated a risk of 1-8 events per 10,000 patients. 

What do all of these studies have in common that I think belies the true incidence of complications associated with peripheral vasoactive drugs? Vigilance. While it’s true that peripheral norepinephrine infusion may not result in serious tissue necrosis when given in the context of a formal clinical study (especially one that takes place in an operating room with continuous monitoring by anesthesia!), what about when the infusion goes unnoticed during a night shift with a high patient to nurse ratio?  In this case, I would argue that the closer to a “real-world experience” we can get with these studies, the better. 

I would also mention that a mentor of mine once theorized the “sunset” of crash central lines as the use of intraosseous catheters became more common in adults in the past decade.  While intraosseous catheters are not without their own complications, it is worth mentioning their role in this conversation as we move forward in thinking about how to transition patients safely from the ED to ICU with several different options for vascular access in lieu of a controlled, sterile central line placement. 

References:

1. Medlej et al. Complications From Administration of Vasopressors Through Peripheral Venous Catheters: An Observational Study.  The Journal of Emergency Medicine 2017; 54(1): 47-53.

2. Pancaro et al. Risk of Major Complications After Perioperative Norepinephrine Infusion Through Peripheral Intravenous Lines in a Multicenter Study. Anesthesia and Analgesia 2019; Published ahead of print.

Marc Sala, MD

Assistant Professor of Medicine

Pulmonary and Critical Care

Northwestern University Feinberg School of Medicine

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Kaskar, S. Ibiebele, A. (2020, Oct 12). Peripheral Vasopressors: Do I need that central line? [NUEM Blog. Expert Commentary by Sala, M]. Retrieved from http://www.nuemblog.com/blog/abdominal-imaging.

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References

1. Cardenas-Garcia J, Schaub KF, Belchikov YG, Narasimhan M, Koenig SJ, Mayo PH. Safety of peripheral intravenous administration of vasoactive medication. Journal of hospital medicine. 2015; 10(9):581-5

2. Tian DH, Smyth C, Keijzers G, et al. Safety of peripheral administration of vasopressor medications: A systematic review. Emergency medicine Australasia. 2019

3. Beck V, Chateau D, Bryson GL et al. Timing of vasopressor initiation and mortality in septic shock: a cohort study. Crit. Care 2014; 18: R97.

Physiologically Difficult Intubations

Written by: Samantha Stark, MD (NUEM ‘20) Edited by: Steve Chukwulebe, MD (NUEM ‘19) Expert Commentary by: Seth Trueger, MD, MPH

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It’s the first few minutes of your shift, and the paramedics roll by your workstation with your first patient, a young woman clutching an inhaler and breathing with every accessory muscle in her body. You direct them to your resuscitation room and they inform you that she has a history of asthma and is having an attack; she’s too exhausted from breathing to verify this, but it seems true. You quickly get her on BiPAP, which mildly improves her work of breathing, but as she becomes drowsy, you obtain a VBG showing a climbing CO2 of 45. You realize that it’s time to intubate this patient, and as you get set up, you collect your thoughts and quickly review everything you’ve heard about intubating asthmatics.

Obstructive Airway Disease

First, remember that asthma is an obstructive airway disease, meaning that there are two main processes to worry about during and after intubation:

• Auto PEEP

• Hypotension secondary to increased intrathoracic pressure from auto PEEP

*Note: auto PEEP is caused by breath stacking in a patient whose expiration is impaired (such as asthma or COPD) – the ventilator initiates a breath before there’s time for full exhalation, and this leads to progressively more volume retained in the lungs, increasing the risk of barotrauma. This can also lead to increased intrathoracic pressure, in turn decreasing preload to the heart and thus causing hypotension.

How to optimize the intubation:

• As you already have this patient on BiPAP, try to preoxygenate as much as possible with this mode of positive pressure

• Consider attempting delayed sequence intubation with ketamine

  • It will maintain the patient’s respiratory drive and may help with BiPAP synchrony and anxiolysis

  • It serves as a bronchodilator

• Use rocuronium for paralysis

  • It will last longer than succinylcholine, and initially help with vent synchrony

  • *Note: remember to fully sedate the patient after intubation, as they won’t tell us that they’re not sedated during their prolonged paralysis

• Decrease the dead space and resistance of your vent by using the largest endotracheal tube feasible

• Frequently reassess the ventilator to ensure that breath stacking is not occurring:

  • Low respiratory rate to allow for exhalation

  • Higher tidal volumes of 6-8 cc/kg IBW

  • Decreased I:E ratio (at least 1:3, may very well need to be longer)

You’ve successfully intubated this patient, and now the lab pages you to let you know that there is a patient in the waiting room with a bicarb of 9. When the patient is wheeled back, his marked tachypnea and work of breathing makes you think he may need to be intubated as well. But he’s so acidotic, and you’re sure you’ve hear something about intubating acidotic people…

Metabolic Acidosis

What you’ve heard is that if you intubate a severely acidotic patient, you’ve killed them. There are two reasons for this:

• It’s very difficult to keep up with their minute ventilation

• There is a transient increase in pCO2 with paralysis (this is normally inconsequential, but in the decompensating acidotic patient, can lead to cardiovascular collapse)

How to optimize the intubation:

• Optimize cardiovascular status as much as possible beforehand

• Bolus fluids

• Consider starting pressors pre-intubation, or having push-dose phenylephrine or epinephrine on hand during intubation

• Match the patient’s minute ventilation

• Ensure adequate pre-oxygenation, using NIPPV

• However, even if oxygenation is not an issue, BiPAP should be used to assess the minute ventilation the patient is maintaining on their own, to help determine what is needed post intubation

• Using delayed sequence technique with ketamine as the induction agent and a short acting paralytic like succinylcholine could theoretically help to avoid apnea as much as possible

• Once intubated, the patient’s pre-intubation minute ventilation (respiratory rate and tidal volume) MUST be matched on the ventilator

• Don’t be surprised to see higher tidal volumes of 8 cc/kg IBW

As you’re sitting down to catch up on notes, a nurse gets your attention to let you know that there is an altered, febrile, tachycardic patient with a pressure of 65/40 tucked away in a bed at the back of the ED that you should probably see right away. As it turns out, this patient needs to be intubated as well.

Shock

As mentioned above, increased intrathoracic pressure from PPV results in decreased venous return to the heart, leading to decreased preload. This obviously has the potential to be quite detrimental to a patient with shock.

How to optimize the intubation:

• Optimize cardiovascular status as much as possible beforehand

• Fluid resuscitation and vasopressors started prior to intubation

• Have push dose pressors available at the bedside should they be needed

• Induction agents:

  • Avoid propofol as it has a propensity to cause hypotension

  • Use etomidate or ketamine

  • Ketamine has been shown to be more hemodynamically stable than etomidate

  • Also, the body should prioritize cerebrovascular blood flow in shock, therefore if etomidate is used, consider decreasing the dose to minimize hemodynamic effects

At this point, you’re too tired to write any notes, so you decide to sit down and, given how your shift has been going so far, do some reading about patients that are dangerous to intubate or difficult to manage on the vent. The first topic you come across is pulmonary hypertension.

Pulmonary Hypertension

Mechanical ventilation is dangerous in these patients due to their inability to tolerate decreased preload, increased afterload, or really any alteration in their tenuous hemodynamics. Unfortunately, in patients with pulmonary hypertension but also systemic hypotension, IV fluids can over-distend the right ventricle and make things worse. There’s not a super reliable way to tell if these patients will be fluid responsive or not; most would suggest a small fluid bolus challenge to see how they respond. There may or may not be time for this prior to intubation, but if there is time, it’s probably worth a try.

How to optimize the intubation:

• Can consider pre-medication with fentanyl:

  • Thought to blunt the hypertensive response to laryngoscopy, similar to head-injured patients

  • In theory, this prevents increased afterload in the pulmonary vasculature

• Induction agent:

  • Consider etomidate

  • Theoretically should have less of an effect on preload than propofol

  • Additionally, less of an effect on afterload than ketamine

• Ventilator settings:

  • Closely monitor plateau pressures to keep them less than 30 cm H2O, to avoid drops in preload due to increased intrathoracic pressure

  • Consider placing an arterial line for frequent ABG checks

  • Both hypercapnia and hypoxia can cause vasoconstriction (increasing afterload in the pulmonary vasculature)

Two days later, while you’re following up on some of your prior patients, you note that the patient in septic shock that you intubated a couple of days ago now has ARDS, and it seems that the inpatient team is having some difficulty managing her on the vent.

ARDS

While this is an area of active research and there are different strategies and methods for helping to improve these patients’ oxygenation, the main thing to remember from the perspective of managing the ventilator is the lung protective strategy:

• Tidal volume 6 cc/kg IBW

• Plateau pressure less than 30 cm H2O

• Minimum PEEP of 5 cm H2O (and remember that these patients may often need significantly higher PEEP) 

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Expert Commentary

Thank you for this review of intubating sick patients - intubating complex physiology is arguably one of the most dangerous things we can do, but there are some straightforward, concrete steps we can take to do it as safely as possible.

For me, the first step is to consider every ED intubation potentially dangerous. Maximize resuscitation (IV fluids; pressors if needed, always ready) and optimize preoxygenation to provide the biggest possible safety net. It’s much more CBA than ABC.

Every patient we intubate in the ED has potential to crump: the sympatholysis from sedation will reduce endogenous catecholamines, and the switch to positive pressure ventilation impairs preload.

Every intubated patient needs post-intubation sedation. I generally default to a fentanyl drip and modify from there (eg add propofol if BP tolerates; add ketamine if not). Do not remove sedation for hypotension; do not use pain as a pressor. That is torture and it is bad. Sedate the patient adequately and if that means more resuscitation (fluid, blood, pressors, etc) then do that too. Do not torture patients to maintain BP.

The easiest tactic to ensure post-intubation sedation is to think of RSI as 3 medications: NMBA, induction agent, and post-intubation sedative. I should not be surprised that I will need post-intubation sedation shortly after intubation.

Perhaps the biggest lesson in ARDS management and prevention in recent years is that nearly everyone potentially benefits from lung protective ventilation, i.e. 6 ml/kg *ideal* body weight. I’ve changed my default tidal volume to 400-450ml (it was 550-600 when I was in med school). Otherwise, ventilation (minute ventilation, or CO2 management) is all about adjusting respiratory rate (my default is 16-18, not 12) as the patient’s height usually does not change in the ED.

Special situations: asthma patients don’t have a big enough tube to exhale properly. Pay special attention, make sure they have sufficient time to exhale (and they may the one group that may benefit from *not* being on 6 ml/kg IBW. Perhaps even more importantly, unlike many other situations, intubation does not fix asthma; it makes it even harder to manage, as even the largest ET tubes are, by definition, smaller than the patient’s natural airway. Maximize NIV and other management options (eg epinephrine) if at all possible.

Acidosis is tough and the key is maximizing ventilation before and after intubation. These patients may need absurd-seeming respiratory rates and regardless of how hypercarbic they are, acidosis does not make patients taller so there is no reason to adjust tidal volume.

Pulmonary hypertension is complex and scary. Prepare beforehand, and work with your intensivists and other relevant specialists.

The most important part of airway management is preparation – not just in the ED, but learning as much as I can beforehand.

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University expert commentator

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Stark, S. Chukwulebe, S. (2020, Oct 5). Physiologically Difficult Intubations. [NUEM Blog. Expert Commentary by Trueger, S]. Retrieved from http://www.nuemblog.com/blog/physiologically-difficult-intubations

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References

1. Ebert TJ, Muzi M, Berens R. Sympathetic responses to induction of anesthesia in humans with propofol or etomidate. Anesthesiology. 1992;76:725-33.

2. Van Berkel MA, Exline MC, Cape KM, et al. Increased incidence of clinical hypotension with etomidate compared to ketamine for intubation in septic patients: a propensity matched analysis. Journal of Critical Care. 2017;38:209-214.

3. Dalabih M, Rischard F, Mosier JM. What’s new: the management of acute right ventricular decompensation of chronic pulmonary hypertension. Intensive Care Med. 2014;40(12):1930-3.

4. Hemmingsen C, Nielson PC, Odorico J. Ketamine in the treatment of bronchospasm during mechanical ventilation. Am J emerg Med. July 1994;12(4):417-420.

5. Eames WO, Rooke GA, Wu RS, Bishop MJ. Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation. Anesthesiology. June 1996;84(6):1307-11.

6. Gragossian A, Asp A, Hamilton R. High Risk Post Intubation Patients. www.emdocs.net/ high-risk-post-intubation-patients/ June 2017

7. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes fo acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308.

8. NIH NHLBI ARDS Clinical Network. Mechanical Ventilation Protocol Summary. www.ardsnet.org/files/ventilator_protocol_2008-07.pdf

9. Marino, Paul L. 2009. The Little ICU Book. Wolters Kluwer Health. Philadelphia, PA.

10. Arbo, John E. 2015. Decision Making in Emergency Critical Care: An Evidence-Based Handbook. Wolters Kluwer Health. Philadelphia, PA.

Vaporizing Lung Injury

Written by: Aaron Wibberley, MD (NUEM ‘22) Edited by: Matt McCauley, MD (NUEM ‘21) Expert Commentary by: Leon Gussow, MD

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Initial post

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Expert Commentary

Although the large cluster of EVALI cases seen last summer and fall has subsided, the known and potential pulmonary problems associated with vaping nicotine or THC products remain an important topic for emergency practitioners and medical toxicologists alike. In a recent update on EVALI, the CDC reported that as of February 18, 2020 a total of 2807 cases had been documented from all 50 states, the District of Columbia, Puerto Rico, and the U.S. Virgin Islands. Among these cases were 68 fatalities. [1]

As this instructive post by Drs. Wibberley and McCauley suggests, many vaping liquids available at retail outlets or on the street are largely unregulated and may contain a witch’s brew of additives and contaminants whose effects on the human respiratory system have not been adequately studied. In addition to glycerin, propylene glycol, and various flavorings, inhaled vapor from these products may also contain toxic metals, formaldehyde, nitrosamines, and acrolein. [2]

One additive strongly linked to EVALI is vitamin E acetate, a synthetic oil used commercially in skin creams, dietary supplements, and multivitamins. Vitamin E acetate has been detected in many non-commercial illicit THC vaping cartridges used by EVALI patients, where it might have been added as a thickener.  It was also found in bronchoalveolar lavage (BAL) fluid drawn from 48 of 51 (94%) confirmed or probable cases of EVALI, but in no such samples from 99 healthy controls. [3,4] Vitamin E acetate may impair the function of pulmonary surfactant. Despite this strong link, the CDC concluded that “evidence is not sufficient to rule out the contribution of other chemicals of concern.’ [5]

As noted in the post, since EVALI is a diagnosis of exclusion, initial clinical efforts should focus on supportive care and ruling-out other potential causes, especially pulmonary infections. Suspecting the diagnosis and establishing a connection to vaping is particularly challenging during flu season or large outbreaks of other respiratory infections. But if EVALI is not considered, a relatively stable patient with early disease may be sent home only to resume vaping. That could lead to disaster. Although new cases of EVALI have not been reported in the last several months, here’s what I think is good practice: any patient with new respiratory complaints should be asked about vaping. If they partake, they should be advised that the practice may be exacerbating their symptoms and counseled to abstain.

References

1. Outbreak of Lung Injury Associated with E-cigarette Use, or Vaping. Centers for Disease Control and Prevention. https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html#latest-information. Accessed May 10, 2020.

2. Ind PW. E-cigarette or vaping product use-associated lung injury. Br J Hosp Med. 2020 Apr;81(4):1-9.

3. Sun LH. Contaminant found in marijuana vaping products linked to deadly lung illnesses, tests show. Washington Post Sept 6, 2019.

4. Blount BC et al. Vitamin E Acetate in Bronchoalveolar-Lavage Fluid Associated with EVALI. N Engl J Med 2020;382:697-705.

5. Ghinai I et al. Characteristics of Persons Who Report Using Only Nicotine-Containing Products Among Interviewed Patients with E-cigarette, or Vaping, Product Use-Associated Lung Injury — Illinois, August-December 2019. MMWR 2020 Jan 24;69(3):84-89.

Dr. Leon Gussow, MD

Assistant Professor of Emergency Medicine, Rush University

Consultant for Illinois Poison Center

Medical Editor, The Poison Review

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Wibberley, A. McCauley, M. (2020, Sept 28). Vaporizing Lung Injury. [NUEM Blog. Expert Commentary by Gussow, L]. Retrieved from http://www.nuemblog.com/blog/vaporizing-lung-injury

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Non Contrast CT Head for the EM Physician

Written by: Philip Jackson, MD (NUEM ‘20) Edited by: Logan Weygandt, MD, MPH NUEM ‘17) Expert Commentary by: Katie Colton, MD

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Relying on in-house radiology reads of imaging is a habit that EM trainees are encouraged to avoid, but one that can be appealing when practicing in a busy, large academic facility with 24-hour radiologist staffing. By reading one’s own images, not only do EM physicians gain skills in diagnostic radiology, which they can employ when an attending radiology read is not readily available but more importantly, the EM physician can correlate history and physical with imaging and help detect subtle pathology. Recent studies have shown that even attending EM physicians are often deficient in reading non-contrast CT scans of the head, however, with minimal training residents have been shown to make significant improvements. [2,3]

An elderly male with a history of hypertension and Fuch’s corneal dystrophy presented to our ED the morning after developing acute on chronic worsening of the blurry vision in his R eye. He suffered from persistent blurry vision but stated that it had suddenly worsened while watching TV the previous night. He then developed a left-sided occipital headache that continued through the following morning. He also noticed that his thinking was “cloudy” and despite being a healthcare professional could not describe his own medical history or list of medications. He described blurriness especially on the right. On visual field confrontation, the patient was found to have a binocular R sided superior quadrantanopsia. The rest of his neurologic exam was unremarkable. As these findings were concerning for stroke specifically in the left temporooccipital region known as Myer’s loop, we obtained a STAT non-contrast head CT.

As the so-called green arrow-signs on the CT image indicate, there was indeed a significant amount of cerebral edema present in the L temporal lobe white matter, which  contains the anterior optic radiations carrying information from the R superior visual field and corresponds to our patient’s deficit. Upon discovering this lesion, our team immediately called our radiology colleagues who confirmed our concern for an acute ischemic infarct.

Like any other task in the ED, reading a head CT should be conducted as efficiently and accurately as possible using a standardized approach. EM residents have been found to be somewhat deficient in our ability to evaluate noncontrast head CTs; however, studies have shown that with adequate training, our skills can significantly improve. [3] Perron et al describe the simple but systematic approach “Blood Can Be Very Bad.” This mnemonic reminds residents to examine for the presence Blood, the shape and consistency of the Cisterns, the texture of the Brain parenchyma, the Ventricles, and the presence of fractures and symmetry of the Bony structures. 

• Blood:  In a non-contrast CT, blood will appear as hyperdense (bright/white) fluid.  As blood ages over weeks, it will become increasingly hypodense (darker).  Blood will present in one of the four following ways:

  • Subarachnoid hemorrhage - A dreaded complication of trauma, a ruptured aneurysm, or an arteriovenous malformation can lead to blood pooling in gravity-dependent areas correlating with the particular arterial defect. Rupture of the anterior communicating artery (ACA) will distribute blood in and around the interhemispheric fissure, suprasellar cistern, and brainstem.  Rupture of the middle cerebral artery (MCA) will distribute blood in the Sylvian and suprasellar cistern, while the posterior cerebral artery (PCA) will also distribute in the suprasellar cistern.

  • Subdural hemorrhage (SDH) – Caused by rupture of the bridging veins, SDHs will present as a crescentic lesions that often cross suture lines. SDHs can be acute, chronic, or mixed, and thus will have varying degrees of density.

  • Epidural Hemorrhage - Another serious complication of trauma, epidural hemorrhages will present as a lenticular (biconvex) areas of hyper-attenuation.     Caused by arterial laceration, with the most common being the middle meningeal artery, epidural hemorrhages can rapidly expand and cause significant and rapid mass effect.  Early identification is thus crucial to reducing mortality from these injuries.

  • Intraparenchymal/intraventricular hemorrhage - Often the result of hypertensive disease in elderly patients or as hemorrhagic strokes, intraparenchymal hemorrhage will most often be located in the basal ganglia. Amyloid angiopathy  (associated with Alzheimer’s dementia) often presents as wedge-shaped areas of hemorrhage in the outer cortex. Trauma leading to brain contusion can also present with intraparenchymal hemorrhage. All intraparenchymal hemorrhages (as well as subarachnoid hemorrhages) can potentially rupture into ventricles causing intraventricular hemorrhage and resultant hydrocephalus.

• Cisterns:  Cisterns are spaces surrounding and cushioning brain matter with cerebrospinal fluid. Each of the four major cisterns should be examined for blood or signs of mass effect: the sylvan fissure (in between temporal and parietal lobes), the circummesencephalic or peripontine cistern, the suprasellar (surrounding the circle of Willis), and the quadrigeminal (atop the midbrain).

• Brain matter: Always examine the gyri for and for distinct grey-white matter differentiation. Ischemic strokes, as in our case, will present with blurring of the grey-white differentiation and cerebral edema (areas of hypodensity).  Early strokes may not be apparent on CT, but after 6 or more hours hypodense lesions should be present with maximal edema occurring approximately 3-5 days after the event. Always examine the falx for midline shift through multiple slices.

• Ventricles:  Examining the third and fourth ventricles is crucial in determining the presence of blood hydrocephalus (dilation) or mass effect (asymmetry).

• Bone:  The bony structures of the head should all be examined for fractures, especially depressed skull fractures, which usually denote intracranial pathology. Also, examining the sphenoid, maxillary, ethmoid, and frontal sinuses for air fluid levels should raise suspicion for a skull fracture. Separate bony windows are available for close examination of these high-density structures. [1]

As our case illustrates, it is crucially important for EM physicians to interpret non-contrast CT scans in a systematic and accurate manner. Clinical correlation is a distinct advantage that we, as emergency physicians, possess and it should be exploited to allow for timely and effective patient care.

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Expert Commentary

Thanks to Drs. Jackson and Weygandt for this great primer to the emergent head CT.  One of the obvious challenges of EM is the breadth of pathology we see, and so having a strategic approach like this one will reveal most of the emergent diagnoses we are looking for.  I will never be a radiologist, but nothing is faster than looking at my own scan. A few thoughts: I start by scrolling a scan through quickly to identify obvious pathology (a bleed, midline shift, etc.) and then try to actively redirect my attention back to a systematic approach. It is easy to hone in on the obvious abnormality and miss smaller but crucial clues. Go through the same progression every time. Get comfortable with finding different windows for your imaging. If you only look in a brain window, you’ll miss critical diagnoses. Symmetry is your best friend - until it is not.  We are remarkably good at picking out asymmetry when looking at imaging, which reveals many of the emergent diagnoses, but keep some of the symmetric processes in the back of your mind.  Many of these can wait for a radiologist’s fine- tooth comb, but a few stand out.  Get used to finding the basilar artery, particularly in your unconscious patient; an acute occlusion in this midline structure is potentially devastating but quick intervention is life-saving. Similarly, acute hydrocephalus merits immediate intervention that can lead to dramatic clinical improvement. Bilateral or midline subdural hemorrhage can also be easily missed; finding these requires a level of comfort with windowing the images and identifying abnormal CSF spaces.

Katie Colton, MD

Instructor, Feinberg School of Medicine

Department of Neuro Critical Care and Department of Emergency Medicine

Northwestern Memorial Hospital

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Philip, J. Weygandt, L. (2020, Feb 10). Non Contrast CT Head for the EM Physician. [NUEM Blog. Expert Commentary by Colton, K]. Retrieved from http://www.nuemblog.com/blog/non-contrast-ct-head-for-the-em-physician

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Other Posts You May Enjoy

References

1. Adams, James, and Erik D. Barton. Emergency Medicine: Clinical Essentials. 2nd ed. N.p.: Elsevier Health Sciences, 2013;633-644.

2. Jamal K, Mandel L, Jamal L, Gilani S. 'Out of hours' adult CT head interpretation by senior emergency department staff following an intensive teaching session: a prospective blinded pilot study of 405 patients. Emergency medicine journal : EMJ. 2014;31(6):467-470.

3. Perron AD, Huff JS, Ullrich CG, Heafner MD, Kline JA. A multicenter study to improve emergency medicine residents' recognition of intracranial emergencies on computed tomography. Annals of emergency medicine. 1998;32(5):554-562.

4. Mayfield Brain & Spine. "Visual field test." Visual Field Test | Mayfield Brain & Spine. N.p., n.d. Web. 19 Dec. 2016.

Canadian Syncope

Written by: Jonathan Hung, MD (NUEM ‘21) Edited by: Jon Anderek (NUEM ‘19) Expert Commentary by: Andrew Moore, MD, MS

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Introduction

Syncope is defined as a brief loss of consciousness that is self-limited. [1] It is a commonly seen chief complaint in the emergency department (ED), consisting of up to 3% of ED visits. [2] There are both benign causes of syncope such as vasovagal syncope and more serious causes such as arrhythmias. By the time these patients present to the ED, they are often asymptomatic and hemodynamically stable. Part of the ED workup and disposition includes risk stratification of these patients that can vary by provider and hospital system. [3] For those who present with high-risk features, ED physicians often recommend admission to the hospital for telemetry monitoring and expedited evaluation with echocardiography. [4] Multiple decision rules, most notably the San Francisco Syncope Rule (SFSR), have been developed to identify syncope patients at risk for poor outcomes. The SFSR takes into account predictors such as a history of heart failure, an abnormal electrocardiogram (ECG), and hypotension to determine 7-day negative outcomes for patients presenting to the ED with syncope. [5] Another study called the Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) includes age over 65 and syncope without prodrome in addition to a history of cardiovascular disease as part of their decision-making tool. [6] Lastly, the Risk Stratification of Syncope in the Emergency Department (ROSE) also takes lab results such as brain natriuretic peptide and hemoglobin into account. [7] Despite the numerous studies examining risk stratification in syncope, each one has limitations and ultimately lack adequate sensitivity and specificity for widespread clinical adoption. A new study published in Academic Emergency Medicine is one of the largest studies to develop a risk tool that identifies adult syncope patients at 30-day risk for serious adverse outcomes defined as a serious arrhythmia, need for intervention to correct arrhythmia, or death. [8]

Study

Thiruganasambandamoorthy V, Stiell IG, Sivilotti MLA, et al. Predicting Short-term Risk of Arrhythmia among Patients With Syncope: The Canadian Syncope Arrhythmia Risk Score. Baumann BM, ed. Acad Emerg Med. 2017;24(11):1315-1326.

Study Design

• Multi-center, prospective, observational cohort study.

• This was a derivation study used to define the parameters of the risk score.

Population

Inclusion criteria:

• Syncope patients presenting within 24 hours of the event

• Adults age ≥16

Exclusion criteria:

• Prolonged loss of consciousness

• Change in mental status from baseline

• Witnessed seizure

• Head trauma or other trauma requiring admission

• Unable to provide history due to alcohol intoxication, illicit drug use or language barrier

• Obvious arrhythmia or nonarrhythmic serious condition on presentation

Intervention protocol

ED physicians and emergency medicine residents were trained to assess standardized variables at the initial ED visit including time and date of syncope, event characteristics, personal and family history of cardiovascular disease, and final ED diagnosis. Other variables were obtained through chart review and included age, sex, vital signs, laboratory results and ECG variables. All ECGs were reviewed by a cardiologist, and abnormal variables were reviewed by a second cardiologist. Physician gestalt for dangerous etiology was also recorded for each patient. Multivariable logistic regression was used for the analysis.

Outcome Measures

Composite of death, arrhythmia, or procedural interventions to treat arrhythmias within 30 days of ED disposition

Results

5,010 patients were enrolled in the study with 106 (2.1%) patients suffering arrhythmia or death within 30 days of ED presentation. Forty-five of the 106 patients suffered their adverse event outside of the hospital. The mean age of the study population was 53.4 (SD 23.0 years) and 54.8% were females. A total of 8 variables were included in the final model:

1. Vasovagal predisposition

2. History of heart disease (CAD, atrial fibrillation/flutter, CHF, valvular abnormalities)

3. Systolic blood pressure <90 or >180 mm Hg at any point

4. Troponin elevation

5. QRS duration >130 msec

6. QTc interval > 480 msec

7. ED diagnosis of cardiac syncope

8. ED diagnosis of vasovagal syncope

The Canadian Syncope Arrhythmia Risk Score had a sensitivity of 97.1% and specificity of 53.4% at a threshold score of 0 based on the study’s internal validation.

Interpretation

This study is the largest, multicenter study assessing predictors of short-term outcomes following initial ED presentation of syncope. The results are similar to previous studies that examined long-term outcomes. One interesting difference is that in prior studies, advanced age was a risk factor in arrhythmia or death, however it did not make the final model in this study. The strengths of this prospective study include the large patient population and that only 6.5% were lost to follow up. Furthermore, developing a simplified risk tool similar to the HEART score for chest pain, it can be easily utilized in the ED to help aid in decision making. Some limitations are that a large portion (54%) of patients did not have a troponin level measured and the study notes that these were usually younger patients with less comorbidities.

In practice, it may be difficult to use this tool if there is provider variation for when cardiac syncope is suspected and when a troponin level is measured. Whether or not the provider diagnoses vasovagal syncope or cardiac syncope is subjective as well, though may serve as a surrogate for “physician gestalt.” These results are helpful in risk stratifying syncope patients especially in regard to short-term outcomes, however this disease process is complex and cannot be oversimplified. Overall, this decision tool at the very least allows ED providers to have a shared decision-making conversation with more robust data to support the various options.

Take Home Points

• The Canadian Syncope Arrhythmia Risk Score is a large, multicenter trial evaluating serious 30-day outcomes following an ED presentation for syncope

• Emergency medicine physicians may consider using this tool to guide their clinical-decision making for syncope patients by offering risk percentages for 30-day adverse events

• At the time this was written a validation study was underway

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Expert Commentary

The management and disposition of syncope has been a conundrum for emergency physicians for decades. In fact, the last 20 years of syncope research have focused on development of a risk stratification score for the ED management of syncope. With the recent external validation of the Canadian Syncope Risk Stratification Score [9] (CSRSS) and the recent publication of the FAINT Score [10] for syncope in older adults, we now have two prospectively derived studies to support risk stratification of the syncope patient. The external validation of the CSRSS showed good sensitivity for low risk patients with a sensitivity of 97.8%.  None of the very low risk or low risk patients in the external validation died or suffered cardiac arrhythmia in 30 days. Based on this if your patient is very low risk or low risk you can safely discharge the patient home with primary care follow up.

In my practice, the CSRSS serves as an adjunct to clinician judgement. Using a risk stratification score is often the impetus for a shared decision-making discussion regarding risk and safe disposition. The results of the external validation study further support clinical use of the CSRSS. 

The FAINT score also shows promise for risk stratification in older patients with syncope and near syncope. This score has not been externally validated, but focuses on the older population that many emergency physicians reflexively admit for cardiac monitoring.

Regardless of which decision score you decide to use in personal practice, most of these patients with unexplained syncope can be safely admitted for a short observation stay.  It is safe to say that we have entered a golden age of syncope decision rules.

Andrew Moore, MD, MS

Emergency Physician and Emergency Care Researcher

Department of Emergency Medicine

Carilion Clinic

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Hung, J, Anderek, J. (2020, Sept 14). Canadian Syncope. [NUEM Blog. Expert Commentary by Moore, A]. Retrieved from http://www.nuemblog.com/blog/canadian-syncope.

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References

1. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. European heart journal 2018;39:1883-948.

2. Sun BC, Emond JA, Camargo CA, Jr. Characteristics and admission patterns of patients presenting with syncope to U.S. emergency departments, 1992-2000. Acad Emerg Med 2004;11:1029-34.

3. Probst MA, Kanzaria HK, Gbedemah M, Richardson LD, Sun BC. National trends in resource utilization associated with ED visits for syncope. The American journal of emergency medicine 2015;33:998-1001.

4. Cook OG, Mukarram MA, Rahman OM, et al. Reasons for Hospitalization Among Emergency Department Patients With Syncope. Acad Emerg Med 2016;23:1210-7.

5. Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Annals of emergency medicine 2004;43:224-32.

6. Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. European heart journal 2003;24:811-9.

7. Reed MJ, Newby DE, Coull AJ, Prescott RJ, Jacques KG, Gray AJ. The ROSE (risk stratification of syncope in the emergency department) study. J Am Coll Cardiol 2010;55:713-21.

8. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 2016;188:E289-98.

9. Thiruganasambandamoorthy V, Sivilotti MLA, Le Sage N, et al. Multicenter Emergency Department Validation of the Canadian Syncope Risk Score. JAMA internal medicine 2020;180:1-8.

10. Probst MA, Gibson T, Weiss RE, et al. Risk Stratification of Older Adults Who Present to the Emergency Department With Syncope: The FAINT Score. Annals of emergency medicine 2019.

Vaginal Self Swabbing

Written by: Alex Herndon, MD (NUEM ‘21) Edited by: Vidya Eswaran, MD (NUEM ‘2020) Expert Commentary by: Matt Klein, MD, MPH

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The Antiquated Pelvic Exam?

As Emergency Medicine physicians the demand to see more patients and expedite turnaround times all while providing quality care and maintaining patient satisfaction is steep. Our attempt to meet these standards is truly tried when posed with having to perform a pelvic exam during a busy shift. Introducing patient self-swabbing: an opportunity to provide quality care while saving precious time and resources.

Chlamydia is the most common infection reported in the United States, particularly among high risk populations such as females ages 15 to 24 [1]. These patients are most likely to present to the Emergency Department for their symptoms, thus it remains the task of the Emergency Medicine physician to screen and diagnose sexually transmitted infections to aid in avoiding complications of infection such as pelvic inflammatory disease, infertility, and ectopic pregnancy [1].

The gold standard for making the diagnosis has traditionally been through the physician-obtained endocervical swab on pelvic exam, an exam than has been shown to be physically and emotionally uncomfortable for a majority of patients, as well as low yield [2]. In 2012 a study at an urban sexual health center on women 16 years of age or older presenting with and without vaginal discharge or bleeding compared self-swabs to physician collected endocervical samples. Self-swabs were more sensitive in detecting chlamydia by nucleic acid amplification tests (NAAT) when compared to physician swabs; compared to self-swabs 1 out of 11 cases were missed by physician collected swabs, an overall 9% miss rate [3]. Patient self-swabs are equivalent to physician swabs in detecting gonorrhea [4] The difference in sensitivity has been attributed to patients having more contact time with the vaginal wall and removing more mucus when self-swabbing compared to when physicians collect samples [5].

Another study performed at two urban teaching hospitals in New York looked at self-swabs versus physician collected swabs in order to assess if self-swabs were as sensitive at diagnosing chlamydia infection within the Emergency Department. Overall self-swabs were 91% sensitive and 99% specific at identifying infection, thus deemed a reasonable alternative to physician collected samples, and implemented as an alternative in order to save time and resources.(6) Currently, self-swabbing is supported by ACOG, AAFP, and the CDC [2, 7, 8].

So why aren’t we doing this more? Inherently, as Emergency Medicine physicians, we are always seeking out the big, the bad, and the ugly, be it a fungating mass, or a case of pelvic inflammatory disease. While the idea of the self-swab shouldn’t obviate the pelvic exam, it can be useful in populations with a history and symptoms suggestive of a sexually transmitted infection, as well as for patients seeking screening after known exposure, or even for patients who refuse to undergo a pelvic exam [2, 7] In addition, patients prefer to obtain self-swabs.(8) While one can argue time is still lost in having to instruct the patient on how to self-swab, its practice in the outpatient clinical setting has become so common that there are numerous resources to aid in patient education, including easy-to-understand diagrams, like the one below, made to adorn bathroom walls [9].

Self swabs have been shown to be less messy, cost-effective, as well as thought to be easy to perform by the majority of patients [10]. When striving to increase efficiency, all the while improving patient care, every second counts. Self-swabbing is one method that can buy back time well-spent.

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Expert Commentary

While this terrific post specifically focuses on the use of self-administered vaginal swabs for the evaluation of cervicitis in the emergency department, the broader utility of the pelvic exam for ED patients has been repeatedly called into question [1, 2]. As you correctly point out, pelvic exams are  uncomfortable, can be distressing for patients, and frequently introduce delays in the patient’s care.

In addition to the evidence supporting self-swabs cited in this post, a 2018 ED-based study suggests the pelvic exam does not increase the sensitivity or specificity of diagnosing chlamydia, gonorrhea, or trichomonas when compared to taking a history alone [3]. While any individual study of this type will be limited by methodologic issues, there does appear to be broad support in the literature for routine use of self-administered swabs.

So why aren’t we doing this? Clinical practice can be slow to change, and that seems to be the case for this topic. I also think this highlights a fundamental feature of the emergency medicine mindset: the emphasis on identifying “bad” conditions, despite an anticipated low likelihood. While I have never personally visualized an unexpected cervical malignancy or traumatic injury during a pelvic exam in the ED, many emergency clinicians fear “missing something” in the absence of direct visualization. But as the 2018 paper highlights, taking an appropriate history should mitigate these concerns. Finally, as this post mentions, patients must be instructed on how to properly perform a self-administered swab, and any education should be appropriate to the patient’s primary language and degree of health literacy.

References

1. Close R, Sachs C, Dyne P. Reliability of bimanual pelvic examinations performed in emergency departments. West J Med. 2001;175(4):240-4.

2. Brown J, Aristizabal J, Fleming R, et al. Does pelvic exam in the emergency department add useful information. West J Emerg Med. 2011;12:208-212.

3. Farrukh S, Sivitz A, Onogul B, et al. The additive value of pelvic examinations to history in predicting sexually transmitted infections for young female patients with suspected cervicitis or pelvic inflammatory disease. Ann Emerg Med. 2018;72(6):703-712.

Dr. Matthew R Klein, MD, MPH

Assistant Professor of Emergency Medicine

Assistant Program Director

Department of Emergency Medicine

Northwestern Memorial Hospital

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How To Cite This Post

[Peer-Reviewed, Web Publication] Herndon, A. Eswaran, V. (2020, Sep 7). Vaginal Self Swabbing. [NUEM Blog. Expert Commentary by Klein, M]. Retrieved from http://www.nuemblog.com/blog/vaginal-self-swabbing.

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Other Posts You May Enjoy

References

1. Wiesenfeld H. Screening for Chlamydia trachomatis Infections in Women. New England Journal of Medicine. 2017; 376(22):2197-2198. doi:10.1056/nejmc1703640.

2. Smith R. The Unnecessary Pelvic Exam. Sinai-Grace Emergency Medicine Residency. http://emsgh.com/wp/the-unnecessary-pelvic-exam-dr-smith/.

3. Schoeman S, Stewart C, Booth R, Smith S, Wilcox M, Wilson J et al. Assessment of best single sample for finding chlamydia in women with and without symptoms: a diagnostic test study. BMJ 2012; 345:e8013

4. Stewart C, Schoeman S, Booth R, Smith S, Wilcox M, Wilson J et al. Assessment of self taken swabs versus clinician taken swab cultures for diagnosing gonorrhoea in women: single centre, diagnostic accuracy study. BMJ 2012; 345:e8107

5. Leon R. Indications and value of self-administered vaginal swabs for STIs and vaginitis. Faculty of Medicine: This Changed My Practice. November 2017. https://thischangedmypractice.com/self-administered-vaginal-swabs-sti-vaginitis/.

6. Berwald N, Cheng S, Augenbraun M, Abu-Lawi K, Lucchesi M, Zehtabchi S. Self-administered Vaginal Swabs Are a Feasible Alternative to Physician-assisted Cervical Swabs for Sexually Transmitted Infection Screening in the Emergency Department. Academic Emergency Medicine. 2009;16(4):360-363. doi:10.1111/j.1553-2712.2009.00359.x.

7. Lunny C, Taylor D, Hoang L, et al. Self-Collected versus Clinician-Collected Sampling for Chlamydia and Gonorrhea Screening: A Systemic Review and Meta-Analysis. Plos One. 2015;10(7). doi:10.1371/journal.pone.0132776.

8. Page C, Mounsey A, Rowland K. PURLs: Is self-swabbing for STIs a good idea?. J Fam Pract. 2013; 62(11):651-3.

9. Self-Collected Vaginal Swabs for Gonorrhea and Chlamydia. NC Sexually Transmitted Diseases Public Health Public Health Program Manual/Laboratory Testing and Standing Orders. 2011.

10. Fielder RL, Carey KB, Carey MP. Acceptability of Sexually Transmitted Infection Testing Using Self-collected Vaginal Swabs Among College Women. Journal of American College Health. 2013;61(1):46-53. doi:10.1080/07448481.2012.750610.

Altitude Illness

Written by: Alex Herndon, MD (NUEM ‘21) Edited by: Danielle Miller, MD (NUEM ‘19) Expert Commentary by: Gabrielle Ahlzadeh, MD

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Expert Commentary

During my four years of residency at sea level, I never treated a patient with altitude sickness. Now, living in Utah and working at a ski clinic where the peak is just over 11,000 feet, I see it almost weekly. Patients tend to be surprised when we diagnose them with acute mountain sickness, either because they are physically fit, otherwise healthy or have been to altitude before and never had symptoms. Educating patients that altitude sickness can affect anyone, regardless of how many marathons they’ve run, is important in ensuring that they follow directions to manage their symptoms. A lot of patients also don’t realize that it takes a few days to develop altitude sickness, and that days 2-3 are usually when symptoms develop. Oftentimes, not sleeping well may be the first symptom. If patients present with symptoms of poor sleep and headaches, it’s important to instruct patients to take it easy and take time to adjust, as well as the importance of staying hydrated and doing their best to get enough sleep. It’s helpful to frame this as days lost on the mountain so patients take their mild symptoms seriously.

Anecdotally, most patients improve pretty rapidly with oxygen administration so when any patient from out of town presents with vague symptoms, our first step in ski clinic is to put them on oxygen . Some patients look pale and ill while others don’t even look sick, and you’re often shocked by their low oxygen saturation. We’ve had fit young patients with oxygen saturations in the 70s who look completely fine, which again, just stresses the importance of obtaining vitals and not being fooled by healthy and fit patients. I’ve seen kids who present with fatigue, vomiting and headache who look sick and then after an hour of oxygen and some fluids, bounce right back to their normal selves.

Obviously it’s important to maintain a broad differential for patients who present with symptoms of altitude sickness, while recognizing that it is a diagnosis that can tie together multiple symptoms. This is especially true in pediatric patients who cannot articulate their symptoms clearly. Checking an initial blood sugar is part of our initial workup, especially in kids. But, if you don’t consider acute mountain sickness, then you won’t be able to make your patient feel better with oxygen, descent or other medications.

From the ski clinic, we often send patients home with portable oxygen tanks mainly to use while they are sleeping, since poor sleep often makes symptoms worse. We treat most patients with both acetazolamide and dexamethasone and frequently recommend they come back to clinic the next day for reassessment. We often recommend that patients sleep at lower altitude and just come up for skiing if possible. For patients with evidence of pulmonary edema, they must descend and are sent to the ER for closer monitoring and treatment. The same would be true with any patient with evidence of altered mental status.

Gabrielle Ahlzadeh, MD

Clinical Assistant Professor of Emergency Medicine

University of Southern California

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Herndon, A. Miller, D. (2020, Aug 31). Altitude Illness. [NUEM Blog. Expert Commentary by Ahlzadeh, A]. Retrieved from http://www.nuemblog.com/blog/altitude-illness

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Lightning Injury

Written by: Sean Watts, MD (NUEM ‘22) Edited by: Michael Conrardy, MD (NUEM ‘21) Expert Commentary by: Gabrielle Ahlzadeh, MD

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Lightning injury has significantly declined in incidence and as a cause of environmental mortality since the 1950’s. However, when it occurs, it can cause significant end-organ damage. It remains the second most common cause of storm related deaths in the United States and accounts for approximately 40-100 deaths per year as well as approximately 300 injuries [2,6]. While rare, it is important to outline the must not miss complications, presentation, and management of lightning injury in the emergency department.

Unlike other forms of electrical injury, lightning is considered direct current and can carry energy ranging from 30,000 to 110,000 amps [1]. The majority of subjects struck by lightning survive, however, 10% of injuries are fatal [2]. Injuries are classified in four ways—direct strike, contact injury, side splash, or ground current [1]. In direct strike, the bolt of lightning makes direct contact with the subject and accounts for approximately 5% of injuries [1]. Contact injuries occur when a subject makes contact with another object that is struck by lightning—i.e. a person is touching a metal pole that is struck [1]. Side splash injuries occur when the current jumps from an object to the subject, and ground current occurs when lightning strikes an object and current travels through the ground to the subject [1]. 

Lightning strikes can cause primarily neurologic injury, but the most common fatal complications are cardiac and respiratory arrest  [2]. This is due to the relative nature of conductivity of the various organs in the body, with lightning following the path of least resistance. The order of conductivity is: nerve > blood > muscle > skin > fat > bone [1]. When lightning strikes, the surge of electricity induces cardiac standstill and apnea due to effects on the medullary respiratory center. Most patients will present with asystole and then degrade into a variety of arrhythmias, most commonly ventricular fibrillation. Interestingly, case-reports have documented successful resuscitations of lightning strike victims after being apneic and pulseless for as long as 15 to 30 minutes. This has lead to the notion that at the scene of a lightning strike, the apparent dead should be treated first.

Approximately 90% of lightning strike victims suffer from superficial skin burns, but less than 5% are deep burns [2]. Common presentations of lightning injury include the Lichtenberg figure that is considered pathognomonic for lightening strike [1].  Neurologic manifestations include keraunoparalysis, which is described as a transient tetraplegia affecting the lower limbs more than the upper limbs, and is often accompanied by sensory loss, pallor, vasoconstriction, and hypertension [2]. The pathophysiology is related to overstimulation of the autonomic nervous system that leads to vascular spasm [1]. Generally, this paralysis resolves within several hours; however, in some patients it can take as long as 24 hours or lead to permanent neurologic injury [2].  Most patients with lightning injury will have a perforated tympanic membrane or develop cataracts immediately following the incident.            

Lichtenberg Figure

If lightning injury does occur, initial management in the emergency department is always focused around initial assessment of airway, breathing, and circulation. An important note is that lightning strike can cause fixed, dilated pupils in the absence of irreversible brain injury and should be taken into consideration when contemplating the termination of resuscitative efforts. In multiple casualty incidents Reverse Triage should be employed—meaning that patients without vital signs or spontaneous respirations should be attended to first [1]. This is because return of spontaneous circulation precedes the resolution of respiratory arrest, and has been demonstrated to be effective, as indicated by a case report in Sequoia and Kings Canyon National Park [4]. An ECG and troponin should be obtained, however, cardiac markers have not been shown to help indicate the extent of injury [1]. Additional diagnostic considerations include obtaining a CK and observing for signs of compartment syndrome, as patients with lightning injury often suffer from rhabdomyolysis. Telemetry using a holter-monitor is the standard of care to observe for subacute ECG changes following injury [1]. In terms of neurologic injury—specifically keraunoparalysis--resolution of symptoms without treatment is common; however, the use of heparin and intravenous hydration has been shown to have efficacy in some cases [2]. If other mechanisms of injury are suspected—e.g. head trauma from a fall—appropriate imaging modalities should be performed on the patient. Most patients with lightning injury should be observed in the emergency department for a minimum of six hours with telemetry. 

Lightning injury is primarily a prevention-based approach. Prevention measures include avoiding tall objects such as ski lifts, cell phone towers, or isolated structures (such as a lone tree in an open field) [1]. If isolated in an austere environment, migration into a cave, dense forest, or a deep ravine is recommended [2]. Another recommended technique is that of “lightning position”. This is performed by sitting or crouching with the knees and feet close together to create a single point of contact with the ground [1]. Other prevention measures include utilizing the 30-30 rule: when lightning is observed, count the time until thunder is heard and if the time is under 30 seconds, seek shelter. The subject should then wait another 30 minutes before leaving shelter [3]. If in a group, individuals should spread themselves out to avoid side splash injury [4]. Signs of acute strike should also be monitored, which includes: a blue haze around objects, static electricity over hair or skin, an ozone smell, and a nearby “crackling” sound [1].       

Lightning Position

Lightning injury, while rare due to increased public education and prevention measures, can present with life threatening injuries. Cardiac dysrhythmias and apnea are the most common life threatening presentations and should be managed according to ACLS guidelines. Take care when considering termination of resuscitative efforts, as patients may present with fixed dilated pupils and there have been remarkable case reports of patients surviving even when found down for a prolonged period of time. Most patients with lightning injury require a basic cardiac work up and can be discharged home after a period of observation on telemetry. 

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Expert Commentary

While lightning injury is an infrequent emergency department presentation, just like most cases in emergency medicine, it can range from insignificant to life threatening. From superficial skin burns to full cardiac arrest, it is important to understand the different types of injuries as well as sequelae. It is also important to remember that because electricity is conducted, lightning can cause deeper injuries that may not be immediately visible. This includes deep skin injuries as well as organ damage. For this reason, basic blood work including cardiac markers and a CPK level should be obtained as well as an ECG. Most injuries will present acutely though injuries such as compartment syndrome and rhabdomyolysis may take longer to develop. These should be suspected with any report of extremity pain or any superficial skin findings or swelling.

Recall that in addition to assessing for effects of lightning injury, also consider other traumatic injuries depending on where the victim was when they were struck. For example, victims may be on top of a building and fall as a result of a lightning strike. Thus, a thorough physical examination and re-examination are necessary. If there is doubt about trauma or unknown scene details, like most things in emergency medicine, assume the worst. Observing patients in the emergency department for a minimum of six hours with telemetry monitoring after any lightning injury will also give you time to reassess the patient and perform an adequate tertiary survey.

Perhaps one of the most important things to remember is that in the setting of mass casualty incidents, victims of lightning injury without vital signs or spontaneous respirations should be attended to first; this is in contrast to all other scenarios where these victims are typically triaged as black triage tags as they are unlikely to survive. Keep this in mind for any EMS personnel who may call in to terminate resuscitations from the field if patients were struck by lightning.

Gabrielle Ahlzadeh, MD

Clinical Assistant Professor of Emergency Medicine

University of Southern California

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How To Cite This Post

[Peer-Reviewed, Web Publication] Watts, S. Conrardy, M. (2020, Aug 24). Lightning Injury [NUEM Blog. Expert Commentary by Ahlzadeh, G]. Retrieved from http://www.nuemblog.com/blog/epistaxis-management.

References

1. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Lightning Injuries: 2014 Update. Chris Davis, MD; Anna Engeln, MD; Eric L. Johnson, MD; Scott E. McIntosh, MD, MPH; Ken Zafren, MD; Arthur A. Islas, MD, MPH; Christopher McStay, MD; William R. Smith, MD; Tracy Cushing, MD, MPH. WILDERNESS & ENVIRONMENTAL MEDICINE, 25, S86–S95 (2014) 

2. Acute transient hemiparesis induced by lightning strike. Rahmani SH1, Faridaalaee G2, Jahangard S3. Am J Emerg Med. 2015 Jul;33(7):984.e1-3. doi: 10.1016/j.ajem.2014.12.031. Epub 2014 Dec 19.

3. Lightning Safety Awareness of Visitors in Three California National Parks. Lori Weichenthal, MD; Jacoby Allen, DO; Kyle P. Davis; Danielle Campagne, MD; Brandy Snowden, MPH; Susan Hughes, MS. WILDERNESS & ENVIRONMENTAL MEDICINE, 22, 257–261 (2011)

4. A Lightning Multiple Casualty Incident in Sequoia and Kings Canyon National Parks. Susanne J. Spano, MD; Danielle Campagne, MD; Geoff Stroh, MD; Marc Shalit, MD WILDERNESS & ENVIRONMENTAL MEDICINE, 26, 43–53 (2015)

5. Curry, M. (2017, May 18). Rosen's Emergency Medicine: Concepts and Clinical Practice. Retrieved from https://www.us.elsevierhealth.com/rosens-emergency-medicine-concepts-and-clinical-practice-9780323354790.html.

6. Electrocution and life-threatening electrical injuries, Spies C, Trohman RG Ann Intern Med. 2006;145(7):531.

Epistaxis Management

Written by: Peter Serina, MD, MPH (NUEM ‘22) Edited by: Danielle Miller, MD (NUEM ‘19) Expert Commentary by: Seth Trueger, MD, MPH

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Expert Commentary

Great overview by Dr. Serina and Dr. Miller of this core EM topic. Epistaxis is in many ways an archetype of the EM problem: it happens to nearly everyone at some point in their lives; most people do fine (and don’t ever need to seek care); most who seek care need a little attention but not much intervention; a small fraction account for most of the work but still generally do well with management; and a tiny fraction of a percent need consultants, may be horribly sick or need rare procedures. There are a lot of potential ways to manage epistaxis (especially those that are only a bit difficult to control) and I find it helpful to distill into fewer options so that things don’t get drawn out.

Much like dysrhythmias, step 1 is stable vs unstable and if they are going to need ENT/IR/airway management, the rest is a waste and don’t dawdle to delay definitive treatment. This is very rare, and most patients go into a stable, stepwise approach:

1) Pinchers

I find most patients either resolved by the time we see them, or simply need some basic nasal pinching. Either way, I use this as an opportunity to counsel patients and *actually demonstrate* what to do if this happens again at home. That includes me pinching their nose in the right place with the right amount of force, and explaining each step so that they understand the rationale (eg blow your nose to get rid of mucus and clots so there are clean surfaces; tilt your head forward so blood doesn’t trickle down your throat and make you release your pinching). I also always put these instructions in their DC paperwork:

If your nose starts to bleed:

1. BLOW YOUR NOSE: this sounds backwards but it will clear out any clot or mucus that will stop a proper clot from forming

2. PINCH YOUR NOSTRILS TOGETHER: hold the soft part of your nose together (just below the bony bridge)

3. DO NOT LET GO FOR 20-30 MINUTES: not even for a second. Do not switch hands. Do not check to see if it's working. Watch an entire TV show on your phone while pinching your nose.

4. TILT YOUR HEAD FORWARD: this will stop blood from running down your throat and making you feel miserable

Things you can do to prevent nosebleeds:

• Keep all foreign bodies out of the nose. This includes fingertips and tissue paper -- do not put anything up your nose

• Use a humidifier at home to help keep your nose skin moist

Return to the ER if you have any concerning symptoms including:

• bleeding that won't stop after 30 minutes of continuous pressure

• weakness

• dizziness

• any other new or concerning symptoms

2) Packers

This is where there is a lot of leeway. If there is something obvious for me to cauterize, I will use some silver nitrate. If I think there is a reasonable chance of success, I will try temporary packing with a TXA-soaked pledget for 10 minutes. If I don’t think that will work, or if that fails, I go straight to a rhinorocket which I also soak in TXA (instead of water); I haven’t seen data for this but it is cheap and safe so why not?

3) Phone calls

If packing fails, ENT consult. Not fun and can take some time (and usually ends up with a recommendation for amox/clav that probably isn’t necessary) but fortunately is rare.

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Serina, P. Miller, D. (2020, Aug 17). Epistaxis Management [NUEM Blog. Expert Commentary by Treuger, S]. Retrieved from http://www.nuemblog.com/blog/epistaxis-management.

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References

Contrast Allergies for the Emergency Medicine Physician

Written by: Niki Patel, MD (NUEM ‘22) Edited by: Jesus Trevino (NUEM ‘19) Expert Commentary by: Seth Trueger, MD, MPH

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Expert Commentary

Thank you for this nice review. The main points I try to keep in mind is that contrast reactions are rare; they are rarely severe; and if a patient did not have a prior severe reaction (especially with pretreatment), it is very unlikely that they will have a severe reaction. Pretreatment probably does little but there are only so many hills to die on and most radiology departments won’t let us completely forego pretreatment. The key is working politely with the radiologists & techs to advocate for the patient and what they need (and if that means a consent form or removing a spurious allergy from the EHR, sure).

In my experience, institutional guideline are generally taken directly from the ACR guidelines (which is the point of specialty guidelines!) and therefore means ED patients need, at most, 4 hour prep; and anyone who hasn’t had a serious airway or anaphylactic reaction can probably be safely scanned with pretreatment as the potential benefit of the scan is higher than the potential risk of a reaction. Any scan that can wait for an 8 or 13 hour prep can be ordered by the admitting team (although I will get the pretreatment ball rolling to help them out). Occasionally a patient needs a scan so urgently they can get immediate doses of steroids and antihistamines and scanned immediately, and with proper SDM & documented consent, we can usually make this happen.

For preps, I try to document all the timing as clearly as possible because shifts change (docs, RNs, radiology techs, etc) and will usually put it clearly in the note & trackboard:

• 0730 methylpred 40mg IV

• 1030 diphenhydramine 50mg IV

• 1130 methylpred 40mg IV + CTPE

In my experience, communicating clearly with everyone involved as to what the plan is is the best way to ensure the plan gets carried out.

And lastly, there is no relation between seafood allergies and contrast allergies; you can’t be allergic to “iodine” (although that is fine as shorthand in the EHR to document a reaction); and there is no cross-allergy between topical povidine-iodine irritation and iodinated contrast (don’t ask).

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University expert commentator

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Patel, N. Trevino, J. (2020, Aug 10). Contrast Allergies for the Emergency Medicine Physician. [NUEM Blog. Expert Commentary by Treuger, S]. Retrieved from http://www.nuemblog.com/blog/contrast-allergies-for-the-em-physician.

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D-dimer for Aortic Dissections and Acute Aortic Syndromes

Written by: Samantha Stark, MD (NUEM ‘20) Edited by: Jesus Trevino (NUEM ‘19) Expert Commentary by: Keith Hemmert, MD

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The diagnosis of aortic dissections and other acute aortic syndromes (AAS) has long plagued the emergency physician due to the non-specific nature of their presenting symptoms and the potentially catastrophic consequences of a missed diagnosis. While there is increasing interest and a growing body of evidence regarding the use of D-dimer in diagnosis, guidance on how to use the D-dimer and comfort in doing so are lacking. In the ADvISED study (Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus D-Dimer for Acute Aortic Syndromes), the safety and efficiency of integrating a pretest probability assessment with D-dimer testing is evaluated.

This was a multicenter prospective observational study that involved 6 hospitals in 4 different countries from 2014-2016, including 1850 patients. They observed the failure rate and efficiency of a diagnostic strategy for ruling out AAS that involved determining pretest probability and combining this with a D-dimer test. The tool used for assessing pretest probability was the aortic dissection detection risk score (ADD-RS, see below) and the D-dimer was considered negative if <500 ng/mL. As above, primary and secondary outcomes were the failure rate and efficiency of this strategy, respectively.

*For each risk category, one point is assigned if one or more risk factors is present. The ADD-RS can therefore vary from 0-3.

For the purposes of this study, it is appropriately assumed that anyone with ADD-RS>1 would need conclusive testing (CTA, TEE, or MRA) to evaluate for AAS regardless of D-dimer level. Therefore, the investigators looked primarily at the integration of negative D-dimer (DD-) testing with ADD-RS=0 or ADD-RS<1 as a possible rule out strategy for AAS. They found that among ADD-RS=0/DD- patients, the failure rate was 0.3% (1/294 patients, 95% CI, 0.1-1.9) and the efficiency in ruling out AAS was 15.9% (1/6 patients, 95% CI, 14.3-17.6); efficiency was computed as the number of patients with negative D-dimer within a risk category divided by the number of enrolled patients). Among ADD-RS<1/DD- patients, the failure rate was also 0.3% (3/924 patients, 95% CI, 0.1-1) and the efficiency was 49.9% (1/2 patients, 95% CI, 47.7-52.2). Of note, as mentioned above, in patients with ADD-RS>1/DD-, the failure rate was 4.4%, corresponding to 1 missed case for every 22 patients, an unacceptable failure rate for a potentially lethal condition.

 While the study’s statistical methods were thorough and sound, and the results quite compelling, there were some issues with the study. Perhaps the most significant of these was that about half of the patients involved in the study did not undergo conclusive diagnosis for AAS (CTA, TEE, MRA, surgery, or autopsy), and their “case adjudication” was based on 2-week follow up data. Of the cases where presence or absence of AAS was determined based on follow up data alone, 13% were determined to have AAS, while 87% were determined to have other explanations for their symptoms. The authors make the arguably legitimate, but unvalidated, assumption that patients with undiagnosed symptomatic AAS would experience some significant clinical event in the 2-week time period from presentation to follow-up. This is further supported by the fact that they did identify 7 cases of AAS during said follow-up period. However, they state that, “nonetheless, we cannot exclude with certainty that in 731 study patients with ADD-RS<1/DD- and a negative 14-day follow-up, few cases of AAS with mild or atypical manifestations might have been missed.”

The authors also point out that there is no established acceptable failure rate of a rule out strategy for AAS. They extrapolate based on prior studies that showed a) the threshold clinical probability of AAS above which the benefits of testing outweigh the risks was 3% and b) similar strategies for PE rule out have been considered acceptable if the upper limit of the 95% CI around the failure rate was <3%, to suggest that the failure rate of 0.3% for both the ADD-RS=0/DD- and the ADD<1/DD- strategies (with upper limits of the 95% CI 1.9% and 1% respectively) could be considered acceptable. That suggestion is intriguing when there is data showing the misdiagnosis rate of AAS reaching as high as 40% and that a mere 2.7% of CTAs obtained to evaluate for AAS yield a positive result.

They conclude that integration of ADD-RS=0 or ADD-RS<1 with negative D-dimer testing may be considered to standardize the diagnostic rule out of AAS, and that expert evaluation and debate are needed to determine whether the outlined strategies are safe and efficient to be recommended and implemented in clinical practice. Below is a flowchart from the paper summarizing their proposed diagnostic approach.   

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Expert Commentary

Thank you for this thoughtful review of the ADvISED trial. Acute Aortic Syndromes (AAS), including aortic dissection, intramural hematoma, ulcer, and rupture, are a challenging set of pathologies for the Emergency Physician. As Drs. Stark and Trevino note in this excellent post, the clinical presentations are often vague, and the mortality rate is high if the diagnosis is missed. The approach to testing for AAS has historically not been based on any validated risk score, but rather on clinical gestalt. As a result of these factors the yield on diagnostic testing for AAS is low, raising concerns about resource use and radiation exposure. Hence, a validated approach to risk stratification, with an acceptably low miss rate, would be a great aid to the Emergency Physician.

It is always important to bear in mind the current standard of care for AAS. The American College of Emergency Medicine currently does not recommend the use of a clinical decision rule alone to rule out AAS, nor does it recommend the use of d dimer alone to rule out AAS. CTA, MRA and TEE are the recommended modalities to diagnose of rule out AAS. [1]  While this study and others may ultimately be a factor in changing ACEP clinical policies, Emergency Medicine house staff should be mindful of the current standard of care when evaluating new diagnostic or risk stratification strategies.

As both the authors and Drs. Stark and Trevino point out, roughly half of the patients in the study did not have gold standard testing for AAS, whether by CTA, MRA, TEE, or autopsy; they were simply assumed to be negative for AAS. While it is difficult to find reliable data on the true mortality rate of untreated AAS, we can use mortality for acute aortic dissections as a proxy. The cumulative 14-day mortality for treated acute aortic dissections (including type A and type B, and both medical management and surgical management) approaches 50%. [2]  One can presume that the mortality rate for untreated disease would be even higher. While this does lend a modicum of logic to the authors’ approach (if they aren’t dead at 14 days, they probably don’t have AAS), it is far from scientific, and fails to meet the bar for the level of evidence required to forego conclusive diagnostic testing for such a lethal pathology.

The highly lethal nature of AAS also raises the question of the acceptable miss rate for a risk stratification tool such as the one proposed in the ADvISED study. As mentioned, a tool like this will inevitably draw comparisons to the PERC rule, which has a failure rate of <2%. However, AAS is a substantially more lethal disease than PE; the 30-day mortality rate of PE is 4%, and the 1-year mortality rate is 13%. [3]  While an apples to apples comparison of the mortality rates of PE and AAS is challenging, the aforementioned 14 day mortality rate for treated AAS (nearly 50% at 14 days) provides a stark contrast. Additionally, AAS encompasses a variety of discrete pathologies, some of which are extraordinarily lethal (e.g., the mortality of an ascending aortic dissection is 1% to 2% per hour after symptom onset). [2]  To use another proxy, the in-hospital mortality rate for type A dissections is 22%, and for type B 13%. [4]  These numbers, of course, discount the (presumably not insignificant) number of patients who die before completing transfer to a quaternary care facility.

All of this is to say that AAS is a much more lethal set of pathologies than PE, and therefore the acceptable failure rate for a risk stratification strategy must be correspondingly lower. The authors report a failure rate for the most conservative option (ADD-RS=0/DD-) of 0.3% - but this must be interpreted in light of the lack of conclusive diagnostic imaging in roughly half of the patients enrolled in the study. Lastly, a comparison of this strategy to clinical gestalt would enable us to evaluate the superiority of this approach to the current one; this is a ripe area for future investigation. In summary, the approach to AAS proposed in the ADvISED study is not ready for widespread implementation, although it is a promising step toward a usable risk stratification strategy. 

References

1. ACEP. ACEP Clinical Policy on Thoracic Aortic Dissection

2. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation. 2005;112(24):3802-3813. doi:10.1161/CIRCULATIONAHA.105.534198

3. Alotaibi GS, Wu C, Senthilselvan A, McMurtry MS. Secular Trends in Incidence and Mortality of Acute Venous Thromboembolism: The AB-VTE Population-Based Study. Am J Med. 2016;129(8):879.e19-879.e25. doi:10.1016/j.amjmed.2016.01.041

4. Evangelista A, Isselbacher EM, Bossone E, et al. Insights from the international registry of acute aortic dissection: A 20-year experience of collaborative clinical research. Circulation. 2018;137(17):1846-1860. doi:10.1161/CIRCULATIONAHA.117.031264

Keith Hemmert, MD

Assistant Professor of Emergency Medicine

Hospital of the University of Pennsylvania

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Other Posts You May Enjoy

References

1. Nazerian P, Mueller C, Matos Soeiro A, Leidel B, Savadeo SAT, Giacino F, Vanni S, Grimm K, Oliveira MT, Pivetta E, Lupia E, Grifoni S, Morello F. Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus D-Dimer for Acute Aortic Syndromes: The ADvISED Prospective Multicenter Study. Circulation. 2018;137:250-258.

2. Righini M et. al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014;311:1117-1124.

3. Perrier A et. al. Multidetector-row computed tomography in suspected pulmonary embolism. N Engl J Med. 2005;352:1760-1768.

4. Van Belle A et. al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. 2006;295:172-179.

5. Sarasin FP et. al. Detecting acute thoracic aortic dissection in the emergency department: time constraints and choice of the optimal diagnostic test. Ann Emerg Med. 1996;28:278-288.

6. Hansen MS et. al. Frequency of an inappropriate treatment of misdiagnosis of acute aortic dissection. Am J Cardiol. 2007;99:852-856.

7. Kurabayashi M et. al. Factors leading to failure to diagnose acute aortic dissection in the emergency room. J Cardiol. 2011;58:287-293.

8. Zhan S et. al. Misdiagnosis of aortic dissection: experience of 361 patients. J Clin Hypertens (Greenwich). 2012;14:256-260.

9. Lovy AJ et. al. Preliminary development of a clinical decision rule for acute aortic syndromes. Am J Emerg Med. 2013;31:1546-1550.

The Timing of Antibiotics in Sepsis

Written by: Jordan Maivelett, MD (NUEM ‘20) Edited by: Andrew Berg (NUEM ‘19) Expert Commentary by: Tim Loftus, MD, MBA

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Introduction

Sepsis. As emergency medicine physicians, we are all quite familiar with the term and its tenets. We all know that early goal directed therapy, including early antibiotics, is an important part of sepsis management and ensuring the best possible outcomes for our patients. You need look no further than international guidelines and subsequent quality benchmarks to see the strong emphasis on timely care. For example, regarding antibiotics, the Surviving Sepsis Campaign Guidelines have a clear recommendation:

It makes sense that early antibiotics are important, but just how important is the timing itself? If we miss the one hour recommendation after “recognizing” sepsis, how does that impact the patient, and is that impact clinically significant? Specifically, how does the timing of antibiotic administration affect mortality in sepsis? Numerous studies have tried to answer that exact question, and I wanted to take the time to review the evidence available to us today.

What we know so far

Kumar et al published one of the first major studies that examined the effects of antibiotic timing on mortality, specifically in patients with septic shock, in 2006. [1] This retrospective study included 2154 patients with septic shock and analyzed the impact of hourly delays in antibiotics on in-hospital mortality. Septic shock was defined as recurrent or persistent hypotension despite fluid resuscitation, and the timing of antibiotics was measured from the onset of said shock. The results were powerful, showing that for each hourly delay after onset of septic shock, in-hospital mortality increased by an average of 7.6% per hour. [1] It is important to note that this was an absolute increase in mortality, and a rather large one at that. Not surprisingly, prompt antibiotic administration in patients with septic shock is paramount. But what about patients with sepsis or severe sepsis who are not in shock?

Many studies have attempted to answer that question, with mixed results. One of the largest and most comprehensive of these studies was a meta-analysis published by Sterling et al in 2015. [2] The meta-analysis included 11 studies totaling 16,178 patients and sought to study the effect of antibiotic timing on in-hospital mortality based on two specific timings: 1) Antibiotic administration less than or greater than three hours from ED triage, and 2) Antibiotic administration less than or greater than one hour from recognition of severe sepsis/septic shock. The latter scenario was included to address the one-hour target recommended in the Surviving Sepsis Campaign Guidelines that was previously mentioned. The study also included an analysis of the effect of delayed antibiotics on mortality in hourly intervals after severe sepsis/septic shock recognition. Interestingly, the study showed no statistical difference in mortality between any of the time points studied. The results are best visualized in Figure 3 from the article, which shows the pooled odds ratios for the two major time points studied. Also included is a summary table that shows the included studies and their associated primary outcomes:

As you can see, the results of the included studies were mixed, with the overall meta-analysis showing no significant difference in in-hospital mortality based on time of antibiotic administration. [2] However, it is worth noting that some of the individual studies demonstrated significance, and the overall trend was toward improved mortality with earlier antibiotics despite no demonstrable significance when pooled together. As previously mentioned, the authors also examined the impact on mortality for each hourly delay after one hour of severe sepsis/septic shock recognition. The pooled odds ratios trended toward improved mortality with earlier antibiotics but again were not statistically significant. [2]

In contrast, Liu et al published a large retrospective study in 2017 that showed significant differences in mortality based on antibiotic timing. [3] Specifically, the study included 35,000 patients from 2010 to 2013 and analyzed the impact of antibiotic timing on in-hospital mortality in patients with sepsis, severe sepsis, and septic shock. Septic shock was defined as patients needing vasopressors or an initial lactate greater than four. Severe sepsis was defined based on signs of end organ dysfunction, including laboratory abnormalities, one or more episodes of hypotension, or need for mechanical or noninvasive ventilation. The remaining patients were included in the sepsis group. The timing of antibiotic administration was measured from initial ED registration. The results were significant, with absolute increases in in-hospital mortality of 0.3%, 0.4%, and 1.8% per hour of delay in antibiotic administration in the sepsis, severe sepsis, and septic shock groups, respectively. [3] Although this is a single, retrospective study and not a meta-analysis, it involves a much larger number of patients in comparison to the Sterling meta-analysis. It is also worth noting that said meta-analysis, though totaling 16,178 patients, was unable to include all studies in each of its analyses, limiting its power.

Overall, the current evidence for timing of antibiotic use in sepsis is mixed, with some studies showing a statistically significant benefit in mortality reduction with early antibiotic use, while others showed a non-significant trend suggestive of the same. Antibiotics are clearly an important part of sepsis management, with earlier antibiotics appearing to be most important in patients with septic shock. However, the data are currently insufficient to specify an exact time point for initiation of antibiotics in septic patients.

So where do we go from here?

Although the data for early antibiotic use are mixed, the signal is clearly suggestive of improved mortality with earlier antibiotic use, and there are future studies that plan to take this to its logical extreme: pre-hospital antibiotics given by EMS. It will be interesting to see the results of such studies and how they juxtapose with the potential harm of unnecessary antibiotics. Of note, this latter concept of the harm of antibiotics given to patients with SIRS criteria who are later found to not have sepsis was not included in the aforementioned articles. Most of the above studies identified patients with sepsis in retrospect, separated them from those that were determined to have an inflammatory or viral process, and studied timing of antibiotics in the septic patients alone. But how did the administration of unnecessary antibiotics affect the non-septic patients? Data exist regarding the impact of antibiotic overuse on a larger scale, hence pushes for antibiotic stewardship and efforts to limit antibiotic resistance. However, patient centered outcomes and how they are affected by the possible increase in antibiotic misuse as we push for earlier antibiotics in sepsis management remains unclear. This is worth including in future analyses, as we need to be able to balance the benefits of giving early antibiotics with the potential risks of inappropriate antibiotic use in the undifferentiated patient.

For example, say it is the peak of flu season, and you have a febrile, tachycardic, normotensive patient with an influenza-like illness that you have yet to see. The patient is currently undifferentiated and could have a viral, bacterial, or inflammatory process. Do you give broad spectrum antibiotics up front, after seeing and examining the patient, or after you have performed an infectious work-up? Even with the above data at our disposal, I think this question is still hard to answer, practice patterns vary, and the only true answer is “it depends.” It is a decision to be made on a case-by-case basis, is dependent on the patient’s presentation and co-morbidities, and the risk of delaying antibiotics must be balanced with the potential harm of giving unnecessary antibiotics. A potential harm that is still relatively unclear.

As of now, all we can say is that the data are mixed. There is a signal suggesting early antibiotics improve mortality in sepsis, and this signal is larger in patients with septic shock. However, not all studies have shown significance, and there is no obvious time point to target based on the current data. Early antibiotics appear to be better, but again, this is for patients with “recognized” sepsis and not necessarily all undifferentiated patients who meet SIRS criteria.

Take Home Points

• Current guidelines and quality measures stress the importance of timely antibiotics after recognition of sepsis.

• Data on antibiotic timing in sepsis are mixed. Early antibiotics seem to affect mortality in sepsis, and this effect appears larger in patients with septic shock. If the patient is hypotensive and there is concern for infection, antibiotics are warranted.

• The risks of inappropriate antibiotic use in the undifferentiated, potentially septic patient and their affect on patient outcomes remain unknown. This warrants study, as the push to give earlier antibiotics risks increasing the rate of unnecessary antibiotic administration.

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Expert Commentary

Thank you to Doctors Jordan Maivelett and Andrew Berg for this well-written and thoughtful overview of the challenging scenario regarding appropriate timing of antimicrobial therapy in sepsis. 

Overall, I would agree with the Take Home Points as espoused by the authors yet would like to highlight a few important considerations:

1. First, and perhaps most importantly, is the recognition that many of the available evidence is retrospective in nature, often analyzing administrative databases collected for other reasons (i.e. not to study outcomes in sepsis).  The study by Liu et al as referenced above falls into this category (so does the notorious Kumar study, by the way).  It is important to understand the inherent limitations in these studies - often, there is very limited information on exact confirmation that there even was an infection, the adequacy of antimicrobial selection, and details concerning source control.  Further, be mindful of studies that adjust data to a large degree.  The Liu study is a good example of this as well as the Ferrer 2014 study.  Additionally, roughly 20% of the time, patients initially thought and treated as septic will be found to have no identifiable source or concern for infection when all said and done (Heffner’s study highlights this; even Kumar’s study had ~20% of pts without evidence of infection).  Further, in the Kumar study, a significant cohort of patients were excluded in whom antimicrobials were administered prior to the development of hypotension.  Fascinatingly, these patients actually did much worse than those who developed hypotension and subsequently were administered antimicrobials.  Who would have hypothesized that? 

2. Second, many prospective studies [2-3,5,7-9] including several that were part of Sterling’s SRMA-- do not conclude that early antimicrobials improve survival.  One study assessed the mortality difference between those administered antimicrobials empirically and those in whom antimicrobials were delayed until objective microbiological confirmation of infection -- a practice which actually was associated with a significant survival benefit. [7]  The MEDUSA study did find that delaying definitive source control (i.e. surgery or CT-guided drainage) >6 hours was associated with increased mortality. An additional prospective study even identified that inadequate antimicrobials were given about 33% of the time, and yet 30d mortality was identical. [4]  An important conclusion from the authors was that “outcome is determined primarily by patient and disease factors.”

3. The authors mention trials analysing the prehospital administration of antimicrobials, a practice akin to mobile stroke units, pre-hospital TPA administration, and the theoretical (but unproven?) benefit of this practice.  The PHANTASi trial was a prospective RCT looking at prehospital antibiotic administration. [1] In short, it did not improve survival compared to usual care. Unfortunately, this study was thought to be impacted by several confounders limiting its impact on practice.

4. Be wary of time to intervention studies.  These are clinically important and impactful research questions, but many clinicians have difficulty in extrapolating the results to pathophysiologic mechanisms of disease.  In other words, time zero of infection is often different - by a significant degree - than time of ED presentation as well as recognition of sepsis.  Expecting an hourly linear relationship between mortality and antibiotics seems dubious. 

5. Triage-based metrics perform poorly, as many patients with sepsis are misclassified initially and many patients don’t even meet diagnostic criteria until well after ED/hospital arrival. [12-13]

Bottom Line

Sepsis survival has increased over the past two decades, from the early phases of the Surviving Sepsis Campaign and the Barcelona Declaration, to Rivers and EGDT, to ProCESS/ProMISe/ARISE and beyond. Largely, this seems to result from structured, multidisciplinary resuscitation, rapid approach to the recognition, diagnosis, and care coordination of this patient population.  Given the complexity of what we understand as the pathophysiology of sepsis, it seems unlikely that a single point in time intervention would have such a profound and pivotal impact on survival. Please don’t delay appropriate antimicrobial therapy particularly in the face of critical illness.  Although I’m not quite at the Mervyn Singer end of the spectrum (“I have yet to be convinced by the prima facie argument that antibiotics make a huge difference to outcomes”) [11], but be mindful of inappropriate, harmful empiric broad spectrum antimicrobials to beat a clock when the diagnosis is still in question.  At the end of the day, retrospective analyses should generate hypotheses, not dictate policy and value-based quality metrics.

Further Reading

1. Alam et al. Prehospital antibiotics in the ambulance for sepsis: a multicentre, open label, randomised trial. Lancet 2018;6(1):40-50. (PHANTASi trial)

2. Bloos et al. Impact of compliance with infection management guidelines on outcome in patients with severe sepsis: a prospective observational multi-center study. Crit Care 2014;18:R42. (MEDUSA)

3. de Groot et al. The association between time to antibiotics and relevant clinical outcomes in emergency department patients with various stages of sepsis: a prospective multi-center study. Crit Care 2015;19:194.

4. Fitzpatrick et al. Gram-negative bacteraemia: a multi-centre prospective evaluation of empiric antibiotic therapy and outcome in English acute hospitals. Clin Microbiol Infect 2016;22:244–251.

5. Kaasch et al. Delay in the administration of appropriate antimicrobial therapy in Staphylococcus aureus bloodstream infection: a prospective multicenter hospital-based cohort study. Infection 2013;41: 979–985. (preSABATO study)

6. Heffner et al. Etiology of illness in patients with severe sepsis admitted to the hospital from the emergency department. Clin Infect Dis 2010;50(6):814-820.

7. Hranjec et al. Aggressive versus conservative initiation of antimicrobial treatment in critically ill surgical patients with suspected intensive-care-unit-acquired infection: a quasi-experimental, before and after observational cohort study. Lancet Infect Dis 2012;12: 774–780.

8. Puskarich et al. Association between timing of antibiotic administration and mortality from septic shock in patients treated with a quantitative resuscitation protocol. Crit Care Med 2011;39: 2066–2071. (EMSHOCKNET).

9. Ryoo et al. Prognostic value of timing of antibiotic administration in patients with septic shock treated with early quantitative resuscitation. Am J Med Sci 2015;349:328–333.

10. Seymour et al. Time to treatment and mortality during mandated emergency care for sepsis. NEJM 2017;376:2235-2244. (the NY State Data)

11. Singer M. Antibiotics for sepsis: does each hour really count, or is it incestuous amplification? Am J Resp Crit Care Med 2017;196(7):800-802.

12. Venkatesh et al. Time to antibiotics for septic shock: evaluating a proposed performance measure. Am J Emerg Med 2013;31(4):680-683.

13. Villar et al. Many emergency department patients with severe sepsis and septic shock do not meet diagnostic criteria within 3 hours of arrival. Ann Emerg Med 2014;64(1):48-54.

Timothy M Loftus, MD, MBA

Assistant Professor of Emergency Medicine

Assistant Medical Director

Department of Emergency Medicine

Northwestern Memorial Hospital

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Other Posts You May Enjoy

References

1. Kumar et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006 Vol. 34, Issue 6.

2. Sterling et al. The Impact of Timing of Antibiotics on Outcomes in Severe Sepsis and Septic Shock: A Systematic Review and Meta- analysis. Crit Care Med. 2015 Vol. 43, Issue 9: 1907–1915.

3. Liu et al. The Timing of Early Antibiotics and Hospital Mortality in Sepsis. Am J Respir Crit Care Med 2017 Vol. 196, Issue 7: 856–863.

Lipid Emulsion Therapy for Local Anesthetic Systemic Toxicity

Written by: Dana Loke, MD (NUEM ‘20) Edited by: Jim Kenny, MD (NUEM ‘18) Expert Commentary by: Patrick Lank, MD, MS

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Local anesthetic systemic toxicity (LAST) is a feared complication of local anesthetic use. Current estimates of LAST toxicity in adults range from 7.5 to 20 per 10,000 peripheral nerve blocks and 4 per 10,000 epidurals.[1] Although rare, this complication can be fatal. Unfortunately, many physicians are unaware of the toxic dose of local anesthetics and are unable to recognize the signs and symptoms of this toxicity.[2] For this reason and the fact that local anesthetic toxicity is rare, by the time this syndrome is identified, patients are often in cardiac arrest or peri-arrest. Thankfully, lipid emulsion such as Intralipid is a safe and effective therapy used to treat LAST.

 How does lipid emulsion therapy work?

Lipid emulsion therapy is an intravenous therapy that binds lipophilic toxins and therefore reverses their toxicity. There are several brand name lipid emulsion therapies, however Intralipid, a soy-based lipid emulsion that contains long-chain triglycerides, is the most commonly used (Figure 1).[3] The ability of lipid emulsion therapy to counteract the toxic effects of local anesthetics was discovered in 1998 by Weinberg et al when it was incidentally found that lab rats pre-treated with an infusion of lipids could withstand larger doses of bupivacaine before arresting.[4] The rats were also more easily resuscitated if given lipid emulsion therapy.[1]  These findings were subsequently confirmed in other laboratories and clinical systemic analyses.[5] Once studied more directly, it was found that intralipid acts as a “sink” by creating a lipid compartment within the plasma that attracts lipophilic compounds, such as local anesthetics, into the lipid sink, which is separate from the aqueous phase of the plasma.[1]

Figure 1: Composition of Various Brands of Lipid Emulsions[1]

How does LAST manifest?

Toxicity is a rare but potentially lethal side effect of local anesthetic. However, since patients often present without any knowledge that they were administered toxic doses of local anesthetic, it is important that the EM physician be cognizant of the signs of this toxicity. Symptoms typically start after a toxic dose of local anesthetic is administered or if local anesthetic is inadvertently administered directly into a vessel instead of subcutaneously (Figure 2). Onset of LAST is typically 30 seconds to 60 minutes after administration of the anesthetic but more often than not occurs within 1-5 minutes.[6]

Figure 2: Maximum Doses and Durations of Various Local Anesthetics[9]

Symptoms of LAST can vary, however there are 5 general ways in which LAST presents.[6] One or all of these manifestations may be present.

• CNS (excitement) – an early manifestation of LAST that often begins with confusion or slurred speech but may include subjective symptoms like metallic taste in the mouth, tinnitus, oral numbness, dizziness, lightheadedness, or visual or auditory disturbances. If not treated promptly, these symptoms often progress to seizures, syncope, coma, respiratory depression, or cardiovascular collapse.

• Cardiovascular – often preceded by CNS symptoms but not always. May include hypertension, tachycardia or bradycardia, arrhythmias, and asystole. Depressed contractility of the heart then leads to progressive hypotension and ultimately cardiac arrest.

• Hematologic – methemoglobinemia, cyanosis

• Allergic – urticaria, rash, and rarely anaphylaxis

• Local tissue response – numbness, paresthesia

The EM physician should maintain a high level of suspicion should a patient present after a same day surgery or procedure with any constellation of these symptoms.

How is lipid emulsion therapy administered?

Once LAST is recognized, the EM physician should immediately consider giving lipid emulsion therapy. An initial dose of 20% lipid emulsion at 1.5 ml/kg or a 100 ml bolus can be administered over a few minutes. This can be repeated after 5 minutes for 2 or more times for persistent hemodynamic instability. The bolus(es) should immediately be followed by a continuous infusion at 0.25-0.5 ml/kg/min.[3] The infusion should run for a minimum of 10 minutes after return of hemodynamic stability, however there are documented reports of recurrent systemic toxicity even after this. For this reason, patients should be admitted for at least 12 hours for observation and additional doses of intralipid as needed for rebound symptoms or hemodynamic compromise.[3] Consultation with your facility’s poison center is also crucial to further guide management.

Efficacy

In terms of efficacy, case reports and systemic analyses have found that lipid emulsion therapy:

• Can reverse both neurologic and cardiac toxicity [5]

• Leads to significantly higher rates of ROSC compared to saline controls in animal models [5]

• Is more effective for witnessed events (for example, brief down time for patients that arrest)5

• Is often effective in patients in which epinephrine, vasopressin, and antiarrhythmic medications did not work

Both hypoxia and acidosis worsen the toxicity of local anesthetics and may inhibit lipid emulsion therapy, so it is imperative that oxygenation and acid-base status are optimized when lipid emulsion therapy is needed.[3, 5]

 Contraindications, Complications, and Special Populations

There are no absolute contraindications to intravenous lipid emulsion therapy and no clinically significant complications documented in the literature. The benefits of lipid emulsion therapy will often outweigh any potential risks in patients with LAST, especially if hemodynamically unstable or coding.

Potential complications of lipid emulsion therapy are mainly related to hypersensitivity. Patients allergic to soybean protein or eggs theoretically may develop allergic or anaphylactic reactions. These reactions should be treated like all other allergic or anaphylactic reactions: with anti-histamines, steroids, and epinephrine as needed. Additionally, there are reported cases of hyperamylasemia however no documented progression to clinical pancreatitis.[3] There are also case reports of extreme lipemia, however even a patient that was inadvertently given 2 L of 20% lipid emulsion did not develop any cardiopulmonary complications.[5] The lipemia however did interfere with standard laboratory tests.[5]

Intralipid is safe in pregnancy and has documented use for treating LAST in term pregnancy.[7] Furthermore, it has documented uncomplicated use in pediatric and neonatal patients.[3, 8]

 Key Points

• Systemic toxicity is a rare but potentially fatal complication of local anesthetic use.

• Lipid emulsion therapy such as Intralipid mitigates the toxic effects of local anesthetics and can reverse both neurologic and cardiac toxicity.

• LAST may manifest initially with CNS symptoms but can progress to seizure, respiratory depression, coma, and cardiovascular collapse.

• An initial bolus of 1.5 ml/kg or 100 ml 20% lipid emulsion followed by an infusion starting at 0.25 ml/kg/min is crucial to reverse toxicity and prevent recurrence.

• Hypoxia and acidosis both worsen LAST and may inhibit lipid emulsion therapy.

• Patients should be admitted in order to monitor for recurrent toxicity.

• There are no contraindications to and minimal side effects of lipid emulsion therapy.

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Expert Commentary

Thank you both for the above thorough review of local anesthetic systemic toxicity (LAST) from the emergency physician perspective! I only want to add a few points to consider when learning more about LAST.

Without going into too much detail, there has been a lot of research done to figure out exactly how lipids aide in the treatment of patients with severe LAST. The lipid sink model is wonderfully understandable and explains many of the clinical and laboratory we see (e.g., a greater decrease in free serum concentration of more lipophilic local anesthetics).  However, there are some other models and theories to be aware of. One I am fascinated by is the “lipid shuttle.” Fundamentally, this describes the phenomenon that lipid therapy will decrease the concentration of local anesthetic at sites of toxicity (i.e., heart and CNS) and increase its concentration in the liver. So instead of lipids acting only as a “sink” to remove a toxin from free availability, it is helping mobilize the toxin to an area where it can go through the process of elimination from the body. Additionally, there are wonderful biochemical explanations (e.g., fatty acid supply, inhibition of nitric oxide release, reversal of mitochondrial dysfunction) to the positive cardiovascular effects seen after lipid treatment in LAST. All of these explanations, it seems, combine to contribute to the hemodynamic response seen in LAST.

Second, I would like to point your readers towards a resource that may help them work through the mechanics of administering lipid rescue therapy in LAST – lipidrescue.org. On that website, one can find links to various protocols, compilations of prior research done on the topic, and much more background on the science of the treatment than I provided above.

Third, in the emergency department, I think you are correct in saying that the most likely source of LAST we would see would come from outpatient surgery centers. A few other clinical scenarios to be aware of would include the following: ingestion of local anesthetics – mostly benzonatate (Tessalon); non-surgical outpatient aesthetic offices that may use topical anesthetics; inappropriate and excessive home use of local anesthetics for pain relief.

Finally, a very brief comment on the use of lipid rescue therapy in non-LAST toxic exposures although that was not the subject of your post. While lipid rescue therapy for LAST has a remarkable record of being effective, that is not yet the case with its use in other toxic exposures. A list of the side effects of lipid rescue therapy includes but is not limited to ARDS, pancreatitis, infection, and significant laboratory interference. While in the setting of severe LAST, the risk: benefit often favors administering lipid rescue, this may not be the case in the setting of non-LAST exposures.  For those non-LAST cases (as well as with LAST cases) in which you are wondering if lipid rescue would be appropriate, I would strongly recommend you call your regional poison center to discuss further focused therapy. 

Patrick Lank, MD, MS

Assistant Professor of Emergency Medicine

Medical Toxicologist

Department of Emergency Medicine

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Loke D, Kenny J. (2020, July 20). Lipid Emulsion Therapy for Local Anesthetic Systemic Toxicity. Expert Commentary by Lank P. Retrieved from http://www.nuemblog.com/blog/lipid-emulsion-therapy

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Other Posts You May Enjoy

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References

1.     Manavi, M. (201). Lipid infusion as a treatment for local anesthetic toxicity: a literature review. AANA Journal, 78(1), 69-78.

2.     Cooper, B.R., Moll, T., & Griffiths, J.R. (2010) Local anaesthetic toxicity: are we prepared for the consequences in the Emergency Department. J Emerg Med, 27(8), 599.

3.     Mercado, P. & Weinberg, G.L. (2011). Local anesthetic systemic toxicity: prevention and treatment. Anesthesiology Clin, 29(2), 233-242.

4.     Weinberg, G.L., VadeBancouer, T., Ramarju, G.A., Garcia-Amaro, M.F., & Cwik, M.J. (1998). Pretreatment or resuscitation with a lipid infusion shifts the dose-response to bupivacaine-induced asystole in rats. Anesthesiology, 88(4), 1071-5.

5.     Weinberg, G.L. (2012). Lipid emulsion infusion: resuscitation for local anesthetic and other drug overdose. Anesthesiology, 117(1), 180-7.

6.     Wadlund, D. (2017). Local anesthetic systemic toxicity. ARON Journal, 106(5), 367-77.

7.     Dun-Chi Lin, J., Sivanesan, E., Horlocker, T.T., & Missair, A. (2017). Two for one: a case report of intravenous lipid emulsion to treat local anesthetic systemic toxicity in term pregnancy. A&A Case Reports, 8(9), 235-7.

8.     Shah, S., Gopalakrishnan, S., Apuya, J., Shah, S., & Martin, T. (2009). Use of intralipid in an infant with impending cardiovascular collapse due to local anesthetic toxicity. J Anesth, 23(3), 439-441.

9. “Missouri Society of Health-System Pharmacists - Overview of Management of Local Anesthetic Systemic Toxicity (LAST) Based on Updated 2017/18 ASRA Practice Guidelines.”

Mood Stabilizer Toxicities

Written by: Justine Ko, MD (NUEM PGY-4) Edited by: Sarah Dhake, MD (NUEM ‘19) Expert Commentary by: Patrick Lank, MD, MS

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Expert Commentary

This is a great summary of the causes, symptoms, work-up, and treatment of two relatively common medications that cause toxicity. In fact, these (along with carbamazepine) are levels I routinely recommend checking in patients with a history of bipolar disorder who come to the emergency department with altered mental status even if they do not report a history of being on these medications. That is because these three medications are very commonly used in the treatment of bipolar disorder and all have quite different treatment courses. In addition to the great summary above, below are some of my usual teaching points about these medications in overdose.

Let's tackle them separately as they are quite different toxicities.

First let's talk about lithium. In almost all medical texts, the tissue distribution of lithium is appropriately identified as being "complex." The easiest way I communicate that with patients, families, and medical learners is that in chronic therapy, lithium forms "stores" of drug in the body and intracellularly. Clinically that is relevant because after performing hemodialysis (HD) for lithium toxicity, you will reliably see an initial drop in lithium concentration followed by elevation approaching pre-dialysis levels if routine HD is performed. Although that could make one feel ambivalent about routinely recommending HD for lithium toxicity, there is suggestion of an alternate advantage of performing HD for lithium toxicity.  Vodovar et al published a study in 2016 showing that patients who met their institutional criteria for HD and had HD performed had significantly fewer neurologic side effects from their toxicity than those who met criteria but did not have HD. So even though it did not impact usual measurements that we would expect HD to influence -- mortality and ICU length of stay -- its performance in this study seems to have been clinically beneficial.

 The other big thing to discuss with lithium toxicity is that there are many known medication interactions with lithium. In short, any medications that impair renal function should not be used in someone on chronic lithium therapy. The main list of those medications includes NSAIDs, ACE inhibitors, ARBs, and thiazide diuretics.

 Most of the unique aspects of valproate toxicity focus on its diagnosis and treatment. In the setting of acute intentional overdose of valproate, one of the most important things for emergency physicians to be aware of is that there can be a delay of peak valproic acid level. There are cases of patients presenting to an emergency department with stated valproate ingestion, initial negative level, then repeat level hours later being in the toxic range. So I recommend serial valproate levels until both down-trending and non-toxic. For treatment, there is a great summary of recommendations by the Extracorporeal Treatments in Poisoning Workgroup (EXTRIP) published online (https://www.extrip-workgroup.org/valproic-acid). In short, consult nephrology for dialysis if the patient is super sick.

 As always, I recommend you consult your regional poison center when you are worried your patient is experiencing medication toxicity. But I hope this infographic and some of my comments helps you understand their recommendations.

 References

1. Vodovar V, et al. Lithium poisoning in the intensive care unit: predictive factors of severity and indications for extracorporeal toxin removal to improve outcome. Clin Tox (Phila) 2016 Sep; 54(8): 615-23.

2.  Lank P and Bryant S. "Valproic Acid" In: Wolfson A, Hendey G, Ling L, Rosen C, Schaider J, Cloutier R (eds.): Harwood-Nuss’ Clinical Practice of Emergency Medicine, 6th edition. Lippincott Williams &amp; Wilkins 2014.

Patrick Lank, MD, MS

Assistant Professor of Emergency Medicine

Medical Toxicologist

Department of Emergency Medicine

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 How To Cite This Post

[Peer-Reviewed, Web Publication] Ko J, Dhake S. (2020, July 13). Mood Stabilizer Toxicities [NUEM Blog. Expert Commentary by Lank P. Retrieved from http://www.nuemblog.com/blog/mood-stabilizer-tox

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Other Posts You May Enjoy

Management of Environmental Heat Injury in the ED

Written by: Sean Watts, MD (NUEM PGY-3) Edited by: Phil Jackson, MD (NUEM ‘20) Expert Commentary by: George Chiampas, DO, CAQSM, FACEP

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Heat related illness has become an increasing source of morbidity and mortality due to environmental injuries from rising global temperatures and increased interest in outdoor activities. The National Oceanic and Atmospheric Administration reported that 2016 was the hottest year on record, and that temperatures were on average 3.2 F° higher than the 20th century averages.[1] Increasing temperatures have manifested in fatal heat waves such as one claiming the lives of 70,000 individuals living in Europe during 2003.[1] The population most subject to these heat waves include the extremes of age and athletes.

Human body temperature is normally set at 37 ° C, and is maintained via the preoptic nucleus of the anterior hypothalamus.[1,2] Hyperthermia results from exposure to an exogenous heat source without altering the hypothalamic set point. As core temperatures elevate during exertion and with exposure to heat, the posterior hypothalamic nucleus signals sympathetic pathways that result in vasodilation of peripheral vascular beds and shunting blood away from gastrointestinal vasculature in order to maximize heat dissipation. Additionally, eccrine sweat glands are cholinergically activated resulting in an evaporative cooling effect. When the duration and magnitude of heat exposure outpace these physiologic mechanisms, the symptoms of heat-related illness become evident and vary from mild heat cramps to severe heat stroke and death.[2]

Heat cramps result from both potassium wasting from persistent utilization of aldosterone in order to maintain a euvolemic state and sodium loss through sweat. Edema can result from increased hydrostatic pressure of the peripheral vasculature. Additionally, syncope and hypotension can manifest due to dehydration, orthostatic pooling of blood, peripheral vasodilation, and a subsequent decrease in cardiac output. Without appropriate treatment, heat exhaustion and the more extreme heat stroke can present.

Heat exhaustion is defined as a core temperature between 37 ° C and 40 ° C with signs and symptoms including intense thirst, weakness, discomfort, anxiety and dizziness.[1,2,6,8] Heat stroke, on the other hand, is defined as a core temperature greater than 40 C° with signs of central nervous system dysfunction. Heat stroke can be further categorized into exertional and non-exertional.[4] The demographic of exertional heat stroke includes athletes, military personal, or young individuals participating in prolonged exercise.[4,8] Non-exertional heat stroke includes the elderly, young children, or individuals with metabolic or cardiac comorbidities that engage in brisk to minor activity at elevated temperatures.[1,4] When the body reaches 40 C° denaturation of proteins, release of pro-inflammatory mediators, and direct activation of the coagulation cascade occurs.[1,2] This can ultimately result in disseminated intravascular coagulation, which is a common complication of heat stroke.[1,4,5] Disruption of the liver and the cerebellum from tissue ischemia, hypoxia, vascular dysfunction, secondary cascade inflammation manifest with elevated liver function tests and ataxia dysmetria, and coma.[1,6]

Summary of the Pathophysiology of Heat Stroke [1]

Treatment of heat related illness in the emergency department rests on appropriate recognition of the severity of disease. For heat syncope and heat cramps, isotonic or hypotonic electrolyte solutions may be administered in addition to actively flexing leg muscles to prevent peripheral pooling of blood.[7,8] Ice packs or cold towels around the neck, axillae and groin can also be used for comfort measures 6. In general, these heat illnesses are self-limiting.

For heat exhaustion and heat stroke, treatments become more aggressive and should be initiated within 30 minutes of recognition of the signs/symptoms.[1,4] These patients often present critically ill and rapid assessment of the patient’s airway, breathing, and circulation is paramount. Caregivers should obtain good IV access, as well as intubate the patient if they are obtunded or in danger of loss of airway protection.[1,6] Broad spectrum critical care labs should be obtained, as well as a CK to assess for evidence of rhabdomyolysis.[5]  Additionally, obtaining an accurate core body temperature is a crucial first step to determine the severity of illness.[1,2,4,5,6] This is best performed through continuous rectal probe monitoring. Rehydration should then be performed, preferably with 1 to 2 L of isotonic fluids.[1,4] Care should be taken to not over-correct hypovolemia as the aforementioned pathophysiology makes this population vulnerable to pulmonary edema.[1] Additionally, care should be taken not to over bolus hypotonic or isotonic solutions as this population, especially those involved in long distance endurance sports like triathlons or marathons, are particularly prone to hyponatremia.[9] If these patients are given too much of these solutions, this can actually exacerbate the hyponatremia. Patients with profound hyponatremia will actually require IV hypertonic solutions or salt tabs.[9]

 Clinicians should next focus on cooling core body temperature. The best treatment for exertional heat stroke is cold-water immersion therapy—where the patient gets placed in a cold body of water.[5,7] This method takes advantage of the high thermal conductivity of water and is most effective when the patient’s clothing is removed. Studies have demonstrated that immersion in an ice-water slurry at 2°C generated cooling rates of 0.35°C/min.[4] Comparatively, allowing hyperthermic subjects to rest in air-conditioned or temperature-controlled rooms only resulted in cooling rates of only 0.03°–0.06°C/min.[4] Evidence regarding an optimal temperature to halt cooling is still under debate, but is thought to be somewhere between 38°C to 39°C, with the fear that overcooling may result in cardiac arrhythmias, especially in the elderly suffering from non-exertional heat stroke.[1,4]

Subject in a cold water-immersion bath after heat- stroke [4]

The use of cold-water immersion therapy in non-exertional heat stroke is still under debate, but the limited evidence shows that evaporative and convective cooling by a combination of cool water spray with continual airflow over the body may be superior, especially in the elderly suffering from non-exertional heat stroke.[4] In many emergency departments, complete cold water immersion therapy may not be readily  available and limited by the placement of cardiac leads, intubation, and IV access, so evaporative and convective cooling methods become first-line for both exertional and non-exertional heat stroke in the emergency department setting should cold water immersion be unavailable.[1,4,5] Should shivering become problematic, benzodiazepines are considered first line therapy.[1,6] In severe or refractory cases the patient may benefit from ECMO.[6]

Evaporative and conductive cooling methods--note the placement of ice packs in axilla, groin as well as the cooling fan overhead [4]

With the rapid increase in heat-related injuries, and projected increase in global warming, researchers are continually seeking new and efficacious treatments. For example, recombinant activated protein C is currently being explored to manage the disseminated intravascular coagulation that may result from heat stroke.[2] Additionally, application of cold packs versus other methods of rapid cooling has been explored. An experimental study published in the journal of Wilderness and Environmental Medicine found that the use of ice packs provided a significantly higher enthalpy change over cold packs—suggesting that ice packs are more efficacious than cold packs when managing heat-injury.[3] Additionally, the study found that application of cold packs or ice packs to locations high in AV anastomoses provided superior cooling rates.[3] Evaporative plus convective cooling units are also under study as an alternative means to cold water immersion for the treatment of non-exertional heat stroke.[5]

Key Points and Summary

• Heat Injury continues to be a major cause of environmental morbidity and mortality, and will likely increase due to rising global temperatures

• Heat Injury exists on a continuum, with heat cramps/syncope on one end and heat exhaustion/stroke on the other end

• Obtain a rectal temperature if you suspect heat exhaustion/stroke, assess ABC’s, get good IV access, and be careful not to over bolus isotonic/hypotonic solutions due to the risk of worsening hyponatremia in athletes

• If feasible, cold water immersion is superior for exertional heat stroke, in the ED setting evaporative and conductive cooling with ice packs can be used

• In severe or resistant cases cardiopulmonary bypass can be effective

table of cooling methods [6]

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Expert Commentary

A great review and reminders of what is a preventable death especially in exertional heatstroke. Unfortunately, still in the United States there are still approximately fifteen to twenty heat-related deaths in athletes annually, mostly seen in august. While there is a spectrum of illness, preventative measures, a high index of concern and management can all mitigate negative outcomes.

In non-exertional heat illness, removal from the environment, addressing the medical condition and or removing any contributing factors is key. Cooling methods and the aggressiveness of cooling are determined by the patient’s mental status and stability. As highlighted, Heat exhaustion presents with headaches, nausea, dizziness, and weakness. Using cooling blankets and cold packs to the groin axilla and circulating fans all are measures in passive cooling. One key element to address as typically a patient presents undifferentiated is to obtain a rectal temperature in a timely fashion as highlighted. Temperatures and glucose in altered mental status patients are critical for efficient management and positive outcomes. There are key studies that highlight that time and duration above 42C lead to higher morbidity including death. 

In athletics, the death of Minnesota football player Korey Stringer in August of 2001 shed greater light on the risks of exertional heatstroke. Since his death, more work and research has been done including best practices in sport to mitigate these outcomes. Across many sports, including Marathons, best practices as outlined in the blog are being implemented pre-hospital. These measures are comparable to the recent out of hospital cardiac arrest best practices of on-sight CPR and utilization of an AED and transport second mantra. In heatstroke “cooling” on sight with ice tub submersion is the current thread being communicated. This messaging is evidenced by a recent EMS consensus paper  that highlights to first-responders the importance of recognizing but also cooling on-sight prior to transport. The delay of cooling and transport times to delay of recognition and cooling in emergency departments may lead to not initiating life-saving rapid cooling beyond the thirty minutes highlighted in the blog.

As you accurately highlighted patients can present differently, however, the key is altered mental status (AMS). Based on experience this can have the forms of patients collapse and obtunded, seizing, irritable and combative to just being confused. Rapid assessments in the right environment with excluding other AMS possibilities will allow the practitioner to respond and manage in a timely fashion. At Northwestern, both Dr. Malik and Dr. Chiampas have published the attached “collapse algorithm” (below) which allows for a quick assessment and possible differential diagnoses. Lastly obtaining a rectal temperature, which at times may be challenging with the combative patient, allows the staff in the Emergency room to objectively determine when to cease cooling. I will share that some of these patients based on their presentation would traditionally be intubated upon arrival. I would caution and remind the practitioner that if you have prepared in advance and can rapidly cool the symptoms are reversible within 10-15 minutes of ice submersion.

Lastly for emergency departments, where out-door events (sporting, festivals or concerts) with the possibility of stimulant use, preparedness is key. At Northwestern, we have secured 100-gallon ice tubs, implemented the collapse algorithm in our trauma bay and on when high-risk events take place to trigger necessary resources. For the Chicago Marathon, Triathlon or major concerts such as Lolla Palooza we order ice to the ER, towels, and prep the tub while educating our staff of the likelihood of these conditions. As we head towards the summer ahead with all of the environmental concerns of climate change and increased temperatures, this blog provides key reminders of the emergency department’s role.

George Chiampas DO CAQSM

Assistant Professor Northwestern University, Feinberg School of Medicine

Departments of Emergency and Orthopedic Surgery

Chief Medical Officer U.S. Soccer

Chief Medical and Safety Officer Bank of America Chicago Marathon

Team Physician Chicago Blackhawks

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How To Cite This Post

[Peer-Reviewed, Web Publication] Watts S, Jackson P. (2020, July 6). Management of Environmental Heat Injury in the ED [NUEM Blog. Expert Commentary by Chiampas G. Retrieved from http://www.nuemblog.com/blog/environmental-heat-injury

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Other Posts You May Enjoy

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References 

1. Heat-Related Illness. Walter F. Atha, MD. Emerg Med Clin N Am 31 (2013) 1097–1108. http://dx.doi.org/10.1016/j.emc.2013.07.012

2. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Heat-Related Illness: 2014 Update. Grant S. Lipman, MD; Kurt P. Eifling, MD; Mark A. Ellis, MD; Flavio G. Gaudio, MD; Edward M. Otten, MD; Colin K. Grissom, MD. WILDERNESS & ENVIRONMENTAL MEDICINE, 25, S55–S65 (2014)

3. Chemical Cold Packs May Provide Insufficient Enthalpy Change for Treatment of Hyperthermia. Samson Phan, MS; John Lissoway, MD; Grant S. Lipman, MD. WILDERNESS & ENVIRONMENTAL MEDICINE, 24, 37–41 (2013)

4. Cooling Methods in Heat Stroke Flavio G.Gaudio MD∗Colin K.Grissom MD†The Journal of Emergency Medicine, Volume 50, Issue 4, April 2016, Pages 607-616

5. Heat Stroke. Alan N. Peiris, MD, PhD, FRCP(London); Sarah Jaroudi, BS; Rabiya Noor, BS. JAMA. 2017;318(24):2503. doi:10.1001/jama.2017.18780

6. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Judith E. Tintinalli, J. Stephan Stapczynski, O. John Ma, Donald M. Yealy, Garth D. Meckler, David M. Cline. Section 16, Chapter 210: Heat Emergencies. http://accessmedicine.mhmedical.com.ezproxy.galter.northwestern.edu/content.aspx?bookid=1658&sectionid=109384117. Accessed June 10, 2019.

7. Heat-Related Illness in Athletes Allyson S. Howe MD, Barry P. Boden, MD First Published August 1, 2007 https://doi-org.ezproxy.galter.northwestern.edu/10.1177/0363546507305013

8. Heat-Related Illnesses. ROBERT GAUER, MD, Womack Army Medical Center, Fort Bragg, North Carolina. BRYCE K. MEYERS, DO, MPH, 82nd Airborne Division, Fort Bragg, North Carolina. Am Fam Physician. 2019 Apr 15;99(8):482-489.

9. Hyponatremia among runners in the Boston Marathon. Almond CS, Shin AY, Fortescue EB, Mannix RC, Wypij D, Binstadt BA, Duncan CN, Olson DP, Salerno AE, Newburger JW, Greenes DS. N Engl J Med. 2005 Apr 14;352(15):1550-6.

Chief Complaint: Sexual Assault

Written by: Logan Wedel, MD (NUEM PGY-3) Edited by: Jason Chodakowski, MD (NUEM ‘20) Expert Commentary by: Erin Lareau, MD

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ED track board reads: 24 F *****, CC: SA

• Unfortunately, this is not an uncommon complaint we see in the ED

• Stay engaged, and prepare for a prolonged patient stay

Sexual Assault has reached Epidemic Proportions in the United States and Globally

19.3% of women and 1.7% of men are raped at some point in their lifetime
Of female rape victims, 78.2% have their first experience of rape before the age of 25 Recent data suggests estimated cost is $122,461 per rape victim .

In one study it was found that alcohol/substance abuse was involved in over 50% of cases.

Only a small proportion of victims present to the emergency department

When they do the we play a vital role in treating injuries, providing prophylaxis, and collecting evidence that can be used to apprehend the attacker

It is not our role to judge the validity of the patient's accusations, to identify the attacker, nor file a police report. The latter is at the patient's discretion.

The process will be time consuming but these patients deserve our full attention: minimize distractions, sit down, provide deep empathy, and give them the space to tell their full story.

Perhaps most importantly you must provide patients with what was violently take from them: a sense of control and safety.

Step 1: Obtain History

1. Time and Location

   • Exact details if able to remember

2. Identity of the Attacker (if known) Number of individuals

   • Possible identifying information

3. Specific Encounter Details - Use Patient Quotes Penetration (vaginal, anal, oral)

   • Ejaculation?

   • Condom use?

   • Use of other foreign bodies?

   • Licking, kissing, biting?

4. Post Assault Activities

   • Shower, urination, defecation?

   • Did they change their tampon, diaphragm, or clothing? Any oral intake or vomiting?

5. Patient's Medical History

   • HIV and Hepatitis B status and vaccination

   • Recent consensual sexual encounters

Step 2: Physical Exam

1. General Physical Exam

   • Immediate and acute interventions always take precedent

2. Pelvic and GU exam

   • Can be done with Evidence Collection Kit If patient consents

3. Detailed skin and soft tissue exam

   • Again can be conducted with Evidence Collection

Step 3: Medical Management

1. Always tend to trauma first

   • Primary and Secondary surveys

   • Workup traumatic injuries (XR / CT / FAST)

2. Baseline Labs and Blood draws

   • CBC, CMP, LFT's, UA, Urine Pregnancy, HIV

3. Offer Medical Advice and Inform patient of Risks, and Potential Prophylaxis Options

   1. High Risk (By Prevalence) --> Empiric Treatment

      • Chlamydia: 528.8 per 100,000 -> Azithromycin 1g PO

      • Gonorrhea:171.9 per100,000 -> Ceftriaxone 250mg IM

      • Trichomonas: 3.1% -> Metronidazole 2g PO

      • Bacterial V.: 29.2% -> Metronidazole 2g PO

   2. Lower Risk--> PEP options

      • HIV: 0.1% vaginal / 2.0% Anal ->

        • Emtricitabine/Tenofovir 200/300mg PO: 1 tab QD

        • Raltegravir 400mg PO: 1 tab BID

      • Hep B: <1% ->

        • Hep B vaccine Series: Now, 1-2m, 4-6m

      • Hepatitis C : < 1% -> No known prophylaxis

      • Syphilis: 9.5 cases per 100,000 ->

        • RPR test at 6wks, 3m, 6m

        • PenicillinG2.4millionUIM

   3. Pregnancy Risks

      • Dependent on Ovulatory Cycle:

      • 3 days before ovulation: 15%

      • 1-2 days before ovulation: 30%

      • Day of ovulation: 12%

      • 1-2 Days after Ovulation: 0%

   4. Emergency Contraception

      • Only if Urine Pregnancy Test Negative

      • Levonorgestrel 1.5mg PO

Step 4: Evidence Collection Kit --Best if within 72 hours

1. Obtain patient consent

   • Verbal Consent to Contact "Rape Victim Advocate"

   • Signed Consent for Sexual Assault Evidence Kit

   • Police must be Contacted//However patient does not have to talk with authorities

     • Patient can also decide to refuse evidence collection at any time

2. AppropriateAttire

   • Gloves,Gown,HairRestraint

3. Collect Articles of Clothing

   • Patient undresses on a sheet, which is supplied in the kit

     • Anything worn at the time of assault

     • Underwear: worn at the time, or up to 72hrs after

   • Individual Articles of Clothing in Separate Areas

     • Place Individually in collection bags, sealed with evidence tape

4. Medical/ForensicDocumentation

   • ObtainedDuringOriginalPatientHistory

   • Key Aspects as Documented Above

5. DetailedPhysicalExam

   • Head to Toe Inspection and Palpation

     • Documentation of ANY Injuries--size, location, color, pattern

     • If Significant, Notify Police to Have Evidence Tech Obtain Photographs

   • Genital/AnalExam

     • Normal Speculum Examination, with Detailed Documentation

     • Note Discharge, Bleeding, Stains, Semen, Foreign Material, Trauma

     • Detailed Description of all Anatomy in Male/Female GU Area

     • Swab Genital / Anal area if Contact Occurred (Lubricate with Sterile Water)

   • Note: Do Not Collect G/C or BV Swabs, Unless Patient is 10 Days out or Having Symptoms

     • Offer Empiric Treatment

Collection Specimens

1. Oral Specimens (4 Total)

   • Swabs: Tongue, Gum Line, Recessed Areas

2. Head Hair Combings

   • From Different Areas of Head

   • Place Comb with the Hair into Paper Sheet

3. Fingernail Specimens

   • Wood Stick to Scrap under Nails

4. Miscellaneous Bite Marks / Stains

   • Swab Area, Label Accordingly

5. Patient Blood on Filter Paper

   • Obtains Drops of Blood for Filter Paper

6. Pubic Hair Combings

   • Comb out Hair onto Supplied Paper

   • Cut Hair if Matted

7. Genital / Anal Swab (4 total)

   • Swab External Genital/Anal Area--Sterile Water to Lubricate

Follow Up Appointments and Safety Assessment

1. Prior to ED Discharge

   • Write for 28 day supply for HIV PEP: Medications as above

2. Primary Care Physician

   • Arrange for close follow up with PMD, ideally within 1 week

   • Send referral if patient is without a primary care physician

3. OB-GYN

   • In order to monitor potential GU trauma

   • HPV / STD surveillance

4. Infectious Disease

   • Within 5 days in HIV PEP is started--Due to potential toxicity

   • Close monitoring of liver function

   • Repeat testing as below

5. On-Going Screening / Laboratory Work --Per ID / Primary Care

   • HIV: at 6 weeks, 3 months, 6 months

   • Hepatitis B: 2nd Vaccination at 3 months / 3rd at 6 months

   • Hepatitis C: at 3-6 months

   • Syphilis: at 6 weeks and 3 months

6. Safety Assessment

   • If at risk for being assaulted again, strongly encourage patient's file a police report although this remains the patient's choice

   • If potentially unsafe going home provide resources for shelters

   • If social work isn't involved yet get them involved

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Expert Commentary 

This is a great summary of current epidemiology and ED clinical practices surrounding the care of sexual assault patients.  To reiterate and expand upon your synthesis: 

•   Sexual assault is an extremely common traumatic injury that is underreported to physicians.

•   Sexual assault victims may have multiple traumatic injuries, acute psychiatric needs, and complex social needs.  A multidisciplinary approach to their care is often helpful, and necessary to reduce further psychological stress associated with the emergency department exam experience after an assault.

•   Recently, the US Department of Justice has published guidelines for training forensic examiners of sexual assault patients, including sexual assault nurse examiners (SANEs) and sexual assault forensic examiner (SAFE). These professionals are specially trained to provide care for sexual assault patients, and to perform the evidence collection.  They are often also trained in forensic photography.  SANEs typically manage the entirety of the patient encounter.  This includes coordination of prophylactic medications and proper follow up.  Illinois currently has a program to train all RNs on the sexual assault exam, and requires a SANE nurse to be available in the ED.

•   There are additionally trained SANE/SAFE providers who also specialize in adolescent/pediatric sexual assault forensics.  These providers should be called upon when available for all children suffering from sexual assault, as there is a higher risk for additional trauma surrounding the exam in these populations.

•   Our job as physicians should therefore focus on:

• Identifying and treating additional medical or traumatic injuries

• Counseling patients on prophylactic medication - as indicated by the exposures which you noted above

• Reviewing expectations and follow up

• Collaborating with our SANE colleagues, volunteer rape victim advocates, pharmacists, police departments, and social workers.

• And as always, we should provide compassion and symptom relief to these patients undergoing an overwhelming traumatic event. 

References:

http://www.illinoisattorneygeneral.gov/victims/sane.html.  Accessed 2/12/2020

https://www.justice.gov/ovw/page/file/1090006/download. Accessed 2/12/2020

Erin Lareau, MD

Assistant Professor of Emergency Medicine

Northwestern Medicine

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How To Cite This Post

[Peer-Reviewed, Web Publication] Wedel L, Chodakowski J. (2020, June 29). Chief complaint: sexual assault [NUEM Blog. Expert Commentary by Lareau E]. Retrieved from http://www.nuemblog.com/blog/chief-complaint-sexual-assault

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Other Posts You May Enjoy

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Resources

1. Avegno, Jennifer, MD et al. "Violence:Recognition,Management,Prevention Sexual Assault Victims in the Emergency Department: Analysis by Demographic and Event Characteristics."
   The Journal of Emergency Medicine, Vol. 37 No. 3. 2009, pp. 328-344

2. “BacterialVaginosisStatistics." Center for Disease Control and Prevention U.S. Department of Health & Human Services.

3. Breiding, Matthew J, PhD eta l. "Morbidity and Mortality Weekly Report: Prevalence and Characteristics of Sexual Violence, Stalking, and Intimate Partner Violence Victimization." Center for Disease Control and Prevention, U.S. Department of Health & Human Services.

4. Chisholm, Christian A. MD, et al. "Intimate Partner Violence and Pregnancy: Epidemiology and Impact." American Journal of Obstetrics & Gynecology Vol 217. No. 2. 2017, pp 141-144.

5. HIV/AIDS:HIVRiskFactors. Center for Disease Control and Prevention, U.S. Department of Health & Human Services.

6. "Northwestern Memorial Hospital Department of Emergency Medicine Clinical Care Guideline: Sexual Assault." https://access.nmh.org/f5-w- 68747470733a2f2f6e6d692e6e6d682e6f7267$$/wcs/blob/1390883725624/clinical -care- guideline-sexual-assault.pdf.

7. "Preventing Sexual Violence." Center for Disease Control and Prevention, U.S. Department of Health & Human Services.

8. "Sexually Transmitted Disease Surveillance 2017: Chlamydia." Center for Disease Control and Prevention U.S. Department of Health & Human Services.

9. "Sexually Transmitted Disease Surveillance 2017: Gonorrhea." Center for Disease Control and Prevention U.S. Department of Health & Human Services.

10. "Sexually Transmitted Disease Surveillance 2017: Syphilis." Center for Disease Control and Prevention U.S. Department of Health & Human Services.

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12. "Trichomoniasis Statistics." Center for Disease Control and Prevention, U.S. Department of Health & Human Services. https://www.cdc.gov/std/trichomonas/stats.htm